title: TCF1 is required for the generation of TCF1highTim3low virus-specific CD8 T cells

status: Public on Dec 22 2016

city: bethesda

first: abdel

last: elkahloun

address: 50 south dr

institute: nih

summary: T-cell exhaustion is frequently observed during chronic viral infection and cancer. How exhausted T cells persist in the presence of immunosuppression is unclear. Here, we showed that virus-specific CD8 T cells differentiate into Tfh-like TCF1highTim3lowBlimp1low progenitors before the chronic phase of viral infection, which persist better than and can give rise to more terminal TCF1lowTim3highBlimp1high cells. Differentiation of TCF1high cells is driven by master regulator TCF1. Cell-intrinsic TCF1 deficiency led to sharp contraction and eventual deletion of virus-specific CD4 and CD8 T cells and uncontrolled viremia

overall_design: 1) tetramer+ WT or Tcf7 cKO CD8 T cells were sorted from day 7 LCMV clone 13 infected mice; 2) tetramer+ Blimp1lowTim3low or Blimp1highTim3high CD8 T cells were sorted from day 7 LCMV clone 13 infected mice; 3) empty MSCV-IRES-GFP control construct or TCF1 over-expression construct transduced P14 cells were sorted from mice on day 8 p.i.. RNA was purified from sorted samples.

first: Abdel

last: Elkahloun

first: Tuoqi

last: Wu

first: Pamela

last: Schwartzberg


title: Microarray expression profiling data for Trp53-null mammary epithelial cells and tumors from a mouse model with a K8+ luminal cell origin

status: Public on Dec 20 2016

city: Boston

first: Zhe

last: Li

state: MA

address: 77 Avenue Louis Pasteur, Room 466

department: Medicine, Genetics Division

country: USA

institute: Brigham and Women's Hospital

summary: Mammary epithelium is hierarchically organized, with multipotent basal mammary stem cells (MaSCs) producing both luminal and basal cells during development or upon transplantation. Recent studies suggested that most breast cancers might originate from luminal cells, and oncogenic events, such as ectopic expression of PIK3CAH1047R, could induce multipotency in committed luminal cells. p53 is the most commonly mutated gene in human breast cancer; in particular, its inactivating mutations are found in most triple-negative breast cancers, raising a question as to whether p53-loss plays a key role in acquisition of MaSC-like properties by luminal cells. By in situ lineage tracing, we found that induced loss of p53 in Keratin 8 (K8)+ luminal cells led to their clonal expansion, in part due to increased proliferation, but did not directly affect their luminal identity. Expansion of luminal cells, in particular oestrogen receptor-positive luminal cells, was observed 3-4 weeks after induced p53-loss, which was accompanied by increased expression of cell cycle genes and downregulation of genes related to immune microenvironment, p53 downstream pathway and apoptosis control. All induced mice eventually developed mammary tumours with 9qA1 (Yap1) amplification and/or 6qA2 (Met) amplification. The resulting tumours exhibited a MaSC-like expression signature and most closely resembled Claudin-Low breast cancer. Overall, these data suggest that although p53 does not directly control the luminal fate, its loss facilitates acquisition of MaSC-like properties by luminal cells and predisposes them to development of mammary tumours with loss of luminal identity. Our data also suggest that Claudin-Low breast cancer can originate from luminal cells, possibly upon transition through a basal-like state.

overall_design: Total RNAs from YFP+ mammary epithelial cells sorted from K8-CreER;Trp53L/L;Rosa26-Stop-YFP or K8-CreER;Rosa26-Stop-YFP females 4 weeks after tamoxifen induction, or from mammary tumors developed in Trp53L/L females or K8-CreER;Trp53L/L females 6-7 months after intraductal injection of Ad-K8-Cre adenovirus or tamoxifen induction, respectively, were prepared and subjected to microarray expression profiling.

first: Ying

last: Xie

first: Luwei

last: Tao


title: Healthy glucocorticoid receptor N363S SNP carriers and metabolic syndrome

status: Public on Dec 07 2016

city: RTP

first: NIEHS

last: Microarray Core

state: NC

address: 111 T.W. Alexander Drive

department: DIR

institute: NIEHS

summary: Differences in gene regulation between healthy glucocorticoid receptor N363S single nucleotide polymorphism carriers and noncarrier controls may underlie the emergence of metabolic syndrome, Type 2 diabetes and cardiovascular disease associated with the N363S polymorphism.

overall_design: Peripheral blood mononuclear cells from healthy glucocorticoid receptor N363S carriers and healthy noncarrier controls were differentiated to macrophages and treated with 100nM dexamethasone or vehicle for 6 hours.  RNA from seven N363S carriers and seven noncarrier controls were used for microarray analysis.

first: Christine

last: Jewell

first: John

last: Cidlowski


title: HDAC6 overexpression effect on mouse ESCs

status: Public on Dec 01 2016

city: Tian Jin

first: Yu

last: Yin

address: 94 Wei Jin Road

country: China

institute: Nankai University

summary: Analysis of mouse ESCs overexpressing HDAC6. Histone deacetylase 6 (Hdac6) was discovered as a deacetylase of α-tubulin and functions in cell migration, immunity and resistance to virus infection in vitro. HDAC6 overexpression ESCs and control ESCs were selected for RNA extraction and hybridization on Agilent microarrays. Results provide insight into the role of HDAC6 in the mouse ESCs.

overall_design: ESCs vs HDAC6-OE ESCs with 2 biological replicates

first: Xiaoxi

last: zhang

first: Lin

last: Liu


title: Identification of genes regulated by Rb in wild-type and SREBP1 KO MEFs

status: Public on Nov 29 2016

city: TSUKUBA CITY

first: Keiichi

last: Minami

state: IBARAKI

address: 17-2 WADAI

department: Tsukuba Research Institute

country: Japan

institute: Ono pharmaceutical

summary: To examine the expressions of Rb regulated genes in wild-type and SREBP1 KO MEFs, we performed DNA microarray analysis.

overall_design: mRNA levels in wild-type and SREBP1 KO MEFs, which were infected with lentivirus expressing Non-target shRNA, or Rb shRNA and cultured with 1%FBS containing media for 24 hours, were analyzed by DNA microarray anaysis.

first: Hayato

last: Muranaka

first: Chiaki

last: Takahashi


title: Induced loss of p53 in mammary luminal cells leads to their clonal expansion and facilitates development of mammary tumours with loss of luminal identity

type:
Expression profiling by array
Genome variation profiling by SNP array

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: Transcriptional profile of Nkx2-5 knockin mutant adult hearts

city: Bar Harbor

first: Mauro

middle: W

last: Costa

address: 600 Main Street

institute: The Jackson Laboratory

summary: Mutations in Nkx2-5 are a main cause of cardiac congenital heart disease. Here we describe a new Nkx2-5 point-mutation murine model, akin to its human counterpart disease generating mutation. Our model fully reproduces the morphological and physiological clinical presentations of the disease and reveals an under-studied aspect of Nkx2-5 driven pathology, a primary right ventricular dysfunction. We further describe the molecular consequences of disrupting the transcriptional network regulated by Nkx2-5 in the heart and show that Nkx2-5 dependent perturbation of the Wnt signaling pathway promotes heart dysfunction through alteration of cardiomyocyte metabolism. Our data provide mechanistic insights on how Nkx2-5 regulates heart function and metabolism, a novel link in the study of congenital heart disease, and confirms that our models are the first murine genetic models to present all spectra of clinically relevant congenital heart disease phenotypes generated by Nkx2-5 mutations in patients.

overall_design: Comparative trancriptional profile of adult heart samples from knockin mouse knockin models containing full deletion of Nkx2-5 or I183M or I183P substitution when compared to control lines where I was changed to I at position 183 (keeping WT gene)

first: Milena

middle: B

last: Furtado


title: Identification of gene expression changes in wild type vs. Pitx2-null cornea.

city: ann arbor

first: philip

last: gage

state: mi

address: 1000 wall street

institute: university of michigan

summary: To identifycandidate PITX2-dependent genes during corneal development, microarray analysis was used to profile gene expression in corneas taken from flash-frozen e12.5 mouse embryos of control (Pitx2+/-) and temporal knockout Pitx2-deficient embryos.

overall_design: To identify candidate PITX2-dependent targets, gene was independently measured in corneal tissue isolated from four embryos of each geneotype.  Corneal tissue isolated from both eyes of a given embryo were pooled and constituted an individual sample pool.

first: Philip

middle: J

last: Gage

first: Alan

last: Dombkowski

first: Chen

last: Kuang


title: Epigenetic stress responses induce muscle stem cell aging by Hoxa9 developmental signals [microarray]

status: Public on Nov 30 2016

city: Jena

first: Friedrich

last: Becker

state: Thuringia

address: Beutenberg Strasse 11

department: Stem cell aging

country: Germany

institute: Leibniz Institute on Aging - Fritz Lipmann Institute

summary:
Background and Aims: Analysis of aging-induced impairments in satellite cells (SCs) – the stem cells of skeletal muscle that are required for its regeneration. Hox genes are known to control stem cell function and development of various tissues.    Methods: We used AlfpCre mice for liver specific deletion of Trp53 in a conditional knockout mouse model to analyze liver carcinogenesis.  Results: Here, we show that liver-specific deletion of p53 in mice consistently induces formation of liver carcinoma depicting bilineal differentiation. Freshly isolated p53-/- liver progenitor cells and hepatocytes exhibit chromosomal imbalances and an enhanced clonogenic capacity compared to p53-positive cells or p21-deficient cells. Primary cultures of hepatocytes and liver progenitor cells from p53-/- mice formed tumors with bilineal differentiation when transplanted into immuno-compromised mice. Together, these results indicate that loss of p53 alone is sufficient to induce primary liver cancer with bilineal differentiation originating from chromosomal instable cultured liver progenitor cells or hepatocytes.   Conclusions: The study shows that p53-dependent checkpoints inhibit transformation of liver progenitor cells and hepatocytes involving p21-independent mechanisms.
In this study the function of the Hoxa9 was analyzed in murine satellite cells.

overall_design: Satellite cells derived from young adult (3-4 month old) C57BL/6J mice were FACS sorted, cultured and transduced with lentiviral particles in order to induce Hoxa9 overexpression. RNA was extracted. Agilent Mouse 8x60K arrays were used.

first: Simon

last: Schwörer

first: Stefan

last: Tümpel

first: K

middle: L

last: Rudolph


title: Gene expression signature of paclitaxel resistance in human esophageal squamous cell cancer cell line

city: Sendai

first: yuriko

last: saiki

state: Miyagi

address: 2-1 Seiryo-machi, Aoba-ku

department: Molecular Pathology

institute: Tohoku University School of Medicine

summary: We examined the microarray-based expression profiles of the cells to identify genes associated with paclitaxel resistance

overall_design: Using parental and paclitaxel resistant cell lines, we studied mRNA transcription levels by microarray analysis to see if there are any of the key molecules for development of acquisition of the paclitaxel resistance.

first: Yuriko

last: Saiki

first: Akira

last: Horii


title: Emergence of Wnt signaling during lung alveologenesis expands and maintains the type 2 alveolar epithelial cell population

city: Philadelphia

first: Michael

middle: Patrick

last: Morley

state: PA

address: 3400 Civic Center Blvd, Bldg 421

department: Penn Cardiovascular Institute

institute: Perelman School of Medicine at the University of Pennsylvania

summary: Alveologenesis is the culmination of lung development and involves the correct temporal and spatial signals to generate the delicate gas exchange interface. Using a novel Wnt signaling reporter system, we have identified a Wnt-responsive alveolar epithelial sublineage arising during alveologenesis called the axin2+ alveolar type 2 cell or AT2Aaxin2. The number of AT2Aaxin2 sublineage cells increases substantially during late lung development, revealing a wave of Wnt signaling during alveologenesis. Transcriptome analysis, in vivo clonal analysis, and ex vivo lung organoid assays reveal that AT2sAaxin2s promote enhanced AT2 cellalveolar growth during generation of the alveolus compared to the overall AT2 population. Activating Wnt signaling in the AT2 lineage results in expansion of the AT2axin2 sublineageAT2s whereas inhibition of Wnt signaling inhibits AT2 cell development and shunts alveolar epithelial development towards the AT1 cell lineage. These findings reveal a novel epithelial sublineage that coordinates Wnt-dependent alveolar growthAT2 expansion required for lung alveologenesis

overall_design: Five samples each from FACS-based isolation of total primary type 2 alveolar epithelial cells from SftpcCreERT2-R26REYFP postnatal day 4 mice after 24 hour lineage tracing and primary type 2 alveolar epithelial cells from postnatal day 4 Axin2CreERT2-TdTomato mice

first: David

last: Frank

first: Tien

last: Peng

first: Jarord

last: Zepp

first: Melinda

last: Snitow

first: Tiffaney

last: Vincent

middle: P

first: Su

last: Zhou

first: Min-Min

last: Lu

first: Edward

middle: E

last: Morrisey


title: Identification of novel genetic markers for mouse yolk sac cells by using microarray analyses

status: Public on Nov 28 2016

city: Shizuoka City

first: Nobuyoshi

last: Shiojiri

address: Oya 836, Suruga-ku

department: Department of Biology

institute: Shizuoka University

summary: The mouse embryonic yolk sac consists of a visceral yolk sac (VYS) and parietal yolk sac (PYS), and may function as a materno-fetal exchange system for nutrients, waste and gas, and physical protector for the embryo/fetus. The present study was undertaken to characterize gene expression of the VYS and PYS endodermal cells, and to identify their novel genetic markers from microarray data with RT-PCR and in situ hybridization analyses.  As a result, Apoa4, Lrp2, Fxyd2, Slc34a3 and Entpd2 were selected as genetic markers of VYS epithelial cells.  These markers were predominantly expressed in VYS epithelial cells, and may involve nutrient uptake and transport of various substances across the VYS membrane. Gkn2 and Pga5 were selected as markers for PYS cells. Gkn2 might be involved in the migration of PYS cells on Reichert’s membrane. Pga5 belongs to the aspartic proteinase family, and is known as ”pepsinogen F.” It may act on degradation of maternal proteins for the nutrient supply to the fetus. The present study also indicated that Mmp1a and Prl7b1 can be used as markers for placenta tissue. The markers reported may be useful for characterization of murine extraembryonic tissues, including yolk sacs and placenta, during development and in culture.

overall_design: Gene expression of the VYS, PYS (endodermal cells and Reichert’s membrane), placenta, liver and small intestine at E12.5 was examined. The numbers of each organ examined are 3, 3, 2, 2 and 1 for the VYS, PYS, placenta, liver and small intestine, respectively.

first: Shinomi

last: Yagi


title: CD1d orchestrates skin cell survival and inflammation in response to UV linking the etiology of sunburn to skin cancer

status: Public on Nov 27 2016

city: Lausanne

first: Angus

last: Moodycliffe

country: Switzerland

institute: Nestlé Reseach Center

summary:
Solar UV represents a ubiquitous environmental physical insult. Thus, to maintain its integrity as an effective barrier, skin must be unusually resistant to cell death. However, UV overexposure causes sunburn1,2 (necrosis and inflammation) and cells that survive harbour damaged DNA, which if not repaired or removed by apoptosis can lead to skin cancer development3-10. CD1d, a transmembrane protein identified in glycolipid antigen presentation11,12 to invariant natural killer T (NKT) cells13,14 is expressed by epithelial cells of most tissues including skin15-17, and shares close homology between humans and mice12. Since CD1d and NKT cells are implicated in regulating UV skin carcinogenesis4,18, we studied susceptibility to UV-induced sunburn in mice either lacking expression of both CD1d and NKT cells or expressing CD1d without NKT cells. Here we show that CD1d, but not NKT cells is necessary for UV to cause sunburn. CD1d causes cells to resist apoptosis in response to UV overexposure as the means to promote cell survival and directs the expression of inflammatory response genes, resulting in tissue destruction and skin inflammation. This previously unknown action of CD1d links the etiology of sunburn to skin cancer.
Keywords = CD1d knockout, UV, sunburn, cancer
Keywords: other

middle: M

first: Bruce

last: German

first: Emmanuelle

last: Lurati

first: Laure

last: Poquet

first: Beatrice

last: Gauthier

first: Michel

last: Demarchez

first: Marlene

last: Schuppli

last: Vilanova

first: James

middle: A

last: Holzwarth

first: Olivier

last: Roye


title: Iron deficiency anemia in mice involves alterations in mitophagy and gene expression in erythroblasts

status: Public on Dec 14 2016

first: Kazuhiko

last: Igarashi

address: Seiryo 2-1

institute: Tohoku University

summary: Since iron deficiency anemia (IDA) is one of the most common diseases in worldwide, it is an essential issue to prevent and to treat the IDA in public healthcare system. However, the precise adaptive responses and their mechanisms of the hematopoietic system induced by iron deficient state are not fully understood. In this study, low iron diet conditions which induce sever iron deficiency anemia in mice were established. Transcriptome analyses in erythroblasts under normal or iron deficient states were performed to describe the pathological details of IDA. Under iron deficient state, extensive gene expression changes and mitophagy disorder were induced during the terminal maturation of erythroblasts. These findings provide a new insight into pathophysiology and molecular biology of IDA and the function of iron as a coordinator of gene expression networks in erythrocyte maturation.

overall_design: Subset II erythroblasts sorted from bone marrow of WT under normal diet or low iron diet after weaning for three weeks or seven weeks. Three biological replication was performed.

first: Hiroki

last: Kato

first: Hiroshi

last: Hada

first: Ari

last: Itoh-Nakadai


title: Expression data of GMDCs with conditioned medium from topotecan-treated E0771 cells

city: Sapporo

first: Yuichi

last: Kitai

address: N12 W6, Kita-ku

department: Faculty of Pharmaceutical Sciences

institute: Hokkaido University

summary: Danger-associated molecular patterns (DAMPs) derived from damaged or dying cells not only elicit inflammation but also potentiate antitumor immune responses. Here, we show that treatment of breast cancer cells with the antitumor agent Topotecan, an inhibitor of topoisomerase I, induces DAMP secretion that triggers dendritic cell activation and cytokine production.

overall_design: To investigate the gene expression of GMDC that were cultured with the conditioned medium from topotecan-treated cells

first: Takumi

last: Kawasaki

first: Takuya

last: Sueyoshi

first: Kouji

last: Kobiyama

first: Ken

last: Ishii

first: Zou

last: Jian

first: Shizuo

last: Akira

first: Taro

last: Kawai


title: Fetal and neonatal hematopoietic progenitors are functionally and transcriptionally resistant to Flt3-ITD mutations.

status: Public on Nov 22 2016

city: St Louis

first: Jeffery

last: Magee

state: Missouri

address: 660 S Euclid Ave.

department: Internal Medicine - Cardiovascular Division

institute: Washington University School of Medicine

summary: Gene expression in control and Flt3-ITD, Stat5 and Runx1 mutant HSCs and HPCs from different developmental stages.

overall_design: HSCs and HPCs were isolated from wild type and FLT3-ITD/+ mice at the indicated ages, or from wild type, Flt3-ITD and Stat5a/b mutant progenitors, or from wild type, Flt3-ITD and Runx1 mutant progenitors.

first: Magee

last: Jeffrey


title: Expression Profile of alloreactive CD8 and CD4 induced regulatory T cells

status: Public on Nov 17 2016

city: Charleston

first: Jessica

last: Heinrichs

state: South Carolina

address: 86 Johnathan Lucas Street

department: Microbiology and Immunology

institute: Medical University

summary: Adoptive natural regulatory T cell (nTreg) therapy has improved the outcome for patients suffering from graft-versus-host disease (GVHD) following allogeneic hematopoietic cell transplantation (allo-HCT). However, fear of broad immune suppression and subsequent dampening of beneficial graft-versus-leukemic (GVL) responses remains a challenge. To address this concern, we generated alloreactive induced Tregs (iTregs) from resting CD4 or CD8 T cells and tested their ability to suppress GVH and maintain GVL responses. We utilized major mismatched and haploidentical murine models of HCT with host-derived lymphoma or leukemia cell lines to evaluate GVH and GVL responses simultaneously. Alloreactive CD4 iTregs were effective in preventing GVHD, but abrogated the GVL effect against aggressive leukemia. Alloreactive CD8 iTregs moderately attenuated GVHD while sparing the GVL effect. Hence, we reasoned that using a combination of CD4 and CD8 iTregs could achieve the optimal goal of allo-HCT. Indeed, the combinational therapy was superior to CD4 or CD8 iTreg singular therapy in GVHD control; importantly, the combinational therapy maintained GVL responses. Cellular analysis uncovered potent suppression of both CD4 and CD8 effector T cells by the combinational therapy that resulted in effective prevention of GVHD, which could not be achieved by either singular therapy. Gene expression profiles revealed alloreactive CD8 iTregs possess elevated expression of multiple cytolytic molecules compared to CD4 iTregs, which likely contributes to GVL preservation. Our study uncovers unique differences between alloreactive CD4 and CD8 iTregs that can be harnessed to create an optimal iTreg therapy for GVHD prevention with maintained GVL responses.

overall_design: 12 samples analyzed, experimental groups (n=3) were CD8+GFP+ and n=3 CD4+GFP+, with GFP being a reporter for Foxp3 expression; controls (n=3) were CD8+GFP- and CD4+GFP-.

first: Jun

last: Li

first: Hung

last: Nguyen

first: Yongxia

last: Wu

first: David

last: Bastian

first: Anusara

last: Daethanasanmak

first: Mohanned

last: Sofi

first: Steven

last: Schutt

first: Chen

last: Liu

first: Junfei

last: Jin

first: Brian

last: Betts

first: Claudio

last: Anasetti

first: Xue-Zhong

last: Yu


title: Expression profiles of prognostic 32-gene liver signature in surgically resected Japanese hepatocellular carcinoma patients

status: Public on Dec 16 2016

city: Dallas

first: Yujin

last: Hoshida

state: TX

address: 5323 Harry Hines Blvd

institute: University of Texas Southwestern Medical Center

summary: Cirrhosis is a milieu that develops hepatocellular carcinoma (HCC), the second most lethal cancer worldwide. HCC prediction and prevention in cirrhosis are key unmet medical needs. Here we have established an HCC risk gene signature applicable to all major HCC etiologies: hepatitis B/C, alcohol, and non-alcoholic steatohepatitis. A transcriptome meta-analysis of >500 human cirrhotics revealed global regulatory gene modules driving HCC risk and lysophosphatidic acid pathway as a central chemoprevention target. Pharmacological inhibition of the pathway in vivo reduced tumors and reversed the gene signature, which was verified in organotypic ex vivo culture of patient-derived fibrotic liver tissues. These results demonstrate the utility of clinical organ transcriptome to enable a new strategy, reverse-engineering precision cancer prevention.

overall_design: Tumor-adjacent liver tissues from 263 Japanese patients who underwent curative surgery for hepatocellular carcinoma.

first: Shigeki

last: Nakagawa

first: Masahiro

last: Kobayashi

first: Toru

last: Beppu

first: Hideo

last: Baba

first: Hiromitsu

last: Kumada


title: Adamts1 Adipocyte Progenitor Cell (APC) expression profile

status: Public on Dec 06 2016

city: Stanford

last: Feldman

state: CA

address: 300 Pasteur Drive

department: Pediatrics

institute: Stanford University

summary: Expression profiling comparing primary adipocyte progenitor cells from Adamts1 transgenic mice to wild-type littermates

overall_design: FACS isolated adipocyte progenitor cells from male mice at 4 weeks of age from the subcutaneous adipose depots of Adamts1 transgenic mice and wild-type controls


title: Identification of potential target neuronal genes of class I histone deacetylase inhibitor treatment.

status: Public on Nov 23 2016

city: Okinawa

first: Gakuya

last: Takamatsu

address: 207 Uehara

department: Department of Molecular & Cellular Physiology

institute: Graduate School of Medicine, University of the Ryukyu

summary: Class I histone deacetylase (HDAC) inhibitors are believed to have positive effects on neurite outgrowth, synaptic plasticity, and neurogenesis in adult brain. However, the downstream targets of class I HDAC inhibitor treatment in neurons are fully unclear. Although class I HDAC inhibitors are thought to broadly promote transcription of many neuronal genes through enhancement of histone acetylation, it is very interesting that the gene set might include as yet unidentified genes that are essential for neuronal survival and function. To identify novel target genes of class I HDAC inhibitor treatment, we screened transcripts of neuronal cultures with microarray using valproate acid.

overall_design: We performed genome-wide comparison of gene expression in mouse primary cerebral cell culture treated with 1 mM valproate acid relative to DMSO control. n = 1.

first: Chiaki

last: Katagiri

first: Tsumuraya

last: Tomoyuki

first: Chigusa

last: Shimizu-Okabe

first: Wakako

last: Toguchi

first: Tomoko

last: Hayakawa

first: Shigeo

last: Wakabayashi

first: Tsuyoshi

last: Kondo

first: Chitoshi

last: Takayama

first: Masayuki

last: Matsushita


title: Transcriptional Response of Male MutaTMMouse Hippocampus to Benzo[a]pyrene (BaP; CAS no. 50-32-8, now also known as benzo[pqr]tetraphene) Exposure

status: Public on Nov 18 2016

city: Ottawa

first: Nikolai

last: Chepelev

state: Ontario

address: 50 Colombine Driveway

department: Environmental Health Science and Research Bureau

country: Canada

institute: Health Canada

summary:
Benzo[a]pyrene (BaP) is a genotoxic carcinogen and a neurotoxicant. The neurotoxicity of BaP is proposed to arise from either genotoxicity leading to neuronal cell death, or perturbed expression of N-methyl-D-aspartate receptor (NMDAR) subunits. To explore these hypotheses, we profiled hippocampal gene expression of adult male MutaTMMouse administered 1, 35, or 70 mg BaP/kg bw per day by oral gavage for three days, by RNA-Sequencing (RNA-Seq), DNA microarrays, and real-time quantitative reverse transcription polymerase chain reaction (RT-PCR) 24 hr post-exposure. RNA-Seq revealed altered expression of zero, 260, and 219 genes (p-value < 0.05, fold-change ≥ ± 1.5) following exposure to the low, medium, and high doses, respectively; 54 genes were confirmed using microarrays.
Microarray and RT-PCR analysis showed increased expression of NMDAR subunits Grina and Grin2a. In contrast, no effects on classical BaP targets, including xenobiotic metabolism and DNA-damage response genes, were found, despite comparable BaP-DNA adduct levels in the cerebellum to those detected in the lung and liver in previous studies. Meta-analysis revealed that BaP-induced transcriptional profiles most closely match those from the hippocampus of transgenic mice that share neurotoxicity observed in BaP-exposed mice (i.e., defects in learning). Overall, our results support that BaP-induced neurotoxicity is more likely to be a consequence of NMDAR perturbation than of genotoxicity, and identify other important genes potentially mediating this adverse outcome.

overall_design: Four (N=4) biological replicates were analyzed for control and BaP-treated (70 mg/kg bw per day, for 3 days) 24 h after the last treatment.

first: Alexandra

middle: S

last: Long

first: Wayne

last: Bowers

first: Rémi

last: Gagné

first: Andrew

last: Williams

first: Byron

last: Kuo

first: David

middle: H

last: Phillips

first: Volker

last: Arlt

first: Paul

last: White

first: Carole

last: Yauk


title: Expression data from intestinal dendritic cells and macrophages of VDTR mice at 4 hours post diphtheria toxin administration

status: Public on Nov 10 2016

city: New York

first: Julie Magarian

last: Blander

state: NY

address: 1425 Madison Avenue, 12-20D

institute: The Icahn School of Medicine at Mount Sinai

summary:
Recognition and removal of apoptotic cells by professional phagocytes, including dendritic cells and macrophages, preserve self-tolerance and prevent chronic inflammation and autoimmune pathologies.  However the diverse array of phagocytes residing within different tissues combined with the necessarily prompt nature of apoptotic cell clearance has made it difficult to study this process in situ.  Thus, the full spectrum of functions executed by tissue resident phagocytes in response to homeostatic apoptosis remains unclear.
We used microarrays to characterize the transcriptome within murine intestinal dendritic cells and macrophages both before and after in situ phagocytosis of apoptotic intestinal epithelial cells.

overall_design: We generated transgenic mice (VDTR) where the primate diphtheria toxin receptor (DTR) fused to enhanced green fluorescent protein (GFP) was driven by the villin promoter enabling expression in intestinal epithelial cells (IEC) of the small and large intestine.  We reasoned that intraperitoneal injection of diphtheria toxin would induce apoptosis specifically in IEC, whose sampling could be monitored by tracking the appearance of GFP within professional phagocytes.  We chose to explore the transcriptome at 4 hour post diphtheria toxin administration as the number of sampleing phagocytes was maximal at this time point.  We found that one dendritic cell subset (herein refered to as CD103) and two macrophage subsets (herein refered to as CD103 CD11b CD64 and CD11b CD64) were responsible for the sampeling of apoptotic IEC.  Cells that sampled were refered to as GFPplus and those that did not were GFPminus.  Data represent five independent experiments with 4 mice per experiment and three biological replicates.

first: Ryan

last: Cummings

first: J

last: Magarian Blander


title: Gene expression from ErbB2KI tumors with a heterozygous or a homoszygous loss of beta-catenin (ctnnb1)

status: Public on Nov 04 2016

city: Montreal

first: Tung

last: Bui

state: Quebec

address: 1160 Pine Ave. W, R507

department: Biochemistry

institute: McGill University

summary:
Beta-catenin controls both cell adhesion and transcription to facilitate ErbB2-driven mammary tumorigenesis
In this study, we used conditional knockout and gene expression approaches to understand global molecular and transciptional changes due to ablation of both functions of beta-catenin.

overall_design: Beta-catenin (ctnnb1) was specifically deleted in the mammary epithelium of ErbB2KI mice. Total RNA was collected from end-burden tumors (flash frozen) and subjected to microarray gene expression.

first: Babette

last: Schade


title: Mutant Kras- and p16-Regulated NOX4 Activation Overcomes Metabolic Checkpoints in Development of Pancreatic Ductal Adenocarcinoma

status: Public on Nov 03 2016

city: Guangzhou

first: Qi

last: Zhao

state: Guangdong

address: No. 651, Dongfengdong Road

department: Medical Oncology

institute: Sun Yat-sen University Cancer Center

summary: That mutational activation of Kras and inactivation of p16 are two signature genetic alterations required for development of PDAC. To elucidate the downstream pathways activated by oncogenic Kras and inactivated p16 in human pancreatic tumorigenesis, we profiled gene expression in HPNE/Kras/shp16 and HPNE/Kras cells using cDNA microarray analysis.

overall_design: We performed cDNA microarray analysis to compare p16 stably silencing cell line originating from HPNE cells with mutant Kras (HPNE/Kras/shp16). HPNE/Kras/shp16 cells placed in the reference channel in hybridization. Expression profiling by array. Two-condition experiment, HPNE/Kras vs. HPNE/Kras/shp16 cells.

first: Huai-Qiang

last: Ju

last: Chiao


title: Expression analysis of WT and Zbtb4 -/- mouse primary fibroblasts

city: Paris

first: Pierre-Antoine

last: Defossez

address: 35 rue Hélène Brion

department: UMR7216 "Epigenetics and Cell Fate"

country: France

institute: CNRS-Université Paris Diderot - Sorbonne Paris Cité

summary: ZBTB4 is a mammalian transcription factor with Zinc fingers and a BTB/POZ domain, which can bind methylated CpGs, as well as certain unmethylated consensus sequences. ZBTB4 is frequently downregulated in human cancers, but it is unclear whether this is a cause or consequence of transformation. To investigate the role of ZBTB4 in normal and pathological conditions, we generated Zbtb4-/- mice

overall_design: To address the Zbtb4 dependant transcriptome, a 10 chip study has been realized using total RNA recovered from wild type and Zbtb4 knock-out mouse embryonic fibroblasts (MEFs)

first: Audrey

last: Roussel-Gervais

first: Olivier

last: Kirsh


title: Role of Ezh2 on Skeletal Development

status: Public on Nov 09 2016

city: Bethesda

first: Julian

middle: CK

last: Lui

state: MD

address: 10 Center Drive

institute: NICHD, NIH

summary:
To study the role of Ezh2 in growth plate, we generated Ezh1 complete knockout, Ezh2 cartilage-specific knockout mice (Ezh1-/-, Col2-cre Ezh2 f/f) and compared it with Ezh2 wildtype littermates (Ezh1 -/-, Col2-cre Ezh2 +/+).
Proliferative zone (PZ) and Hypertrophic zones (HZ) of proximal tibial growth plate were dissected from 3-day old mice by laser capture microdissection and RNA were isolated by pico pure RNA isolation kit

overall_design: Total 24 samples, 6 WT PZ vs 6 KO PZ; 6 WT HZ vs 6 KO HZ, to identify genes up- or down-regulated upon deletion of Ezh2 expression in the growth plate

middle: C

first: Weiping

last: Chen


title: Expression data from NKG2A/C/E+ and negative CD4 effectors after influenza A infection

status: Public on Nov 08 2016

city: Worcester

first: Allen

middle: Minh

last: Vong

address: 368 Plantation Street

department: Pathology

institute: University of Massachusetts Medical School

summary:
CD4 T cells can differentiate into a hetergenous population of effector T cells. A population of cytotoxic CD4 T cells can be generated against influenza challenge, however identifying these cells have been challenging. The expression of NKG2A/C/E on CD4 T cells identifies CD4 T cells with cytotoxic potential thus allowing further characterization of this subset of CD4 effector cells.
Microarray analysis comparing cytotoxic CD4 T cells versus non-cytotoxic CD4 T cells reveals unique differences in localization between these populations in the lung after influenza A challenge.

overall_design: Congenically marked TCR transgenic HNT CD4 T cells were adoptively transferred into naïve host mice which were subsequently infected with influenza A virus[strain A/PR8]. At day 7 post infection, the transferred CD4 effectors were flow sort purified from lungs based on their expression of NKG2A/C/E. RNA was extracted and hybridized on Affymetrix arrays.

first: Susan

last: Swain


title: Vulnerability of Purkinje cells induced from spinocerebellar ataxia type 6 patient-derived iPS cells [2]

city: Hirakata

first: Keiko

last: Muguruma

address: 2-5-1 Shinmachi

department: Graduate School of Medicine

institute: Kansai Medical University

summary: Spinocerebellar ataxia type 6 (SCA6) is a dominantly inherited neurodegenerative disease characterized by loss of Purkinje cells in the cerebellum. It is known to be caused by CAG trinucleotide repeat expansion in CACNA1A, the gene that encodes Cav2.1, α1A subunit of P/Q-type calcium channel. However, the pathogenic mechanism and effective therapeutic treatments are still unknown. Here we have succeeded in generation of mature Purkinje cells that carry the patient genes by combining patient-derived iPS cell and self-organizing culture technologies. Patient-derived Purkinje cells exhibited upregulation of whole Cav2.1 protein while downregulation of its C-terminal fragment and the transcriptional targets TAF1 and BTG1. We further demonstrate that patient Purkinje cells exhibit thyroid hormone depletion-dependent degeneration, which can be suppressed by two compounds, thyroid releasing hormone and Riluzole. Thus we have constructed an in vitro disease model recapitulating both ontogenesis and pathogenesis. This model would be useful for pathogenic investigation and drug screening

overall_design: Examination of mRNA profile in iPSC-derived neural progenitors from 4 repeated healthy control and 4 repeated cases

first: Hideshi

last: Kawakami

first: Hiroyuki

last: Kitajima

first: Ayaka

last: Nishiyama

first: Yoshiki

last: Sasai

first: Haruhisa

last: Inoue


title: Expression data from CD8 T cells from LCMV-Clone13 infected mice after two weeks of control or anti-PD-L1 treatment

status: Public on Oct 31 2016

city: Philadelphia

first: E

middle: JOHN

last: WHERRY

address: 421 Curie Blvd,354 BRB II/III

department: Systems Pharmacology       and Translational Therapeutics,Institute for Immunology

institute: University of Pennsylvania

summary:
Blocking PD-1 can reinvigorate exhausted CD8 T cells (TEX) and improve control of chronic infections and cancer. One potential advantage of this immunotherapy is durable protection if immune memory can be established. It is unclear, however, whether blocking PD-1 can reprogram TEX into effector (TEFF) or durable memory T cells (TMEM). Here, we found reinvigoration of TEX by PD-L1 blockade caused re-acquisition of some features of TEFF, but minimal memory development.
We used microarray analysis to profile exhausted cells from anti-PD-L1 mice after two weeks of treatment to study if PD-L1 blockade caused re-acquistion of some feature of effector or memory cells.

overall_design: CD8 T cells from spleens 1-2 days after the final treatment (after receiving 5 total treatments of anti-PD-L1) were enriched by magnetic beads (CD8 negative selection kit, Stem Cell Technologies) and Dbgp276+ CD8 T cells were sorted on a FACSAria (BD). Four biological replicates were performed for each treatment  group and the transcriptional profiles were studied using affymetrix microarrays

first: Kristen

last: Pauken

last: Wherry


title: Early Inhibition of Fatty Acid Synthesis Reduces Generation of Memory Precursor Effector T cells in Chronic Infection

status: Public on Nov 05 2016

city: Galveston

first: Robin

last: Stephens

state: Texas

address: 301 University Blvd

department: Infectious Diseases

institute: UTMB

summary: Understanding the mechanisms of CD4 memory T cell (Tmem) differentiation in malaria is critical for vaccine development. However, the metabolic regulation of CD4 Tmem differentiation is not clear, particularly in persistent infections. In this study, we investigated the role of fatty acid synthesis (FAS) in Tmem development in Plasmodium chabaudi chronic mouse malaria infection. We show that T cell-specific deletion, and early pharmaceutical inhibition of acetyl coA carboxylase 1, the rate limiting step of FAS, inhibit generation of early memory precursor effector T cells (MPEC). To compare the role of FAS during early differentiation or survival of Tmem in chronic infection, a specific inhibitor of acetyl coA carboxylase 1, 5-(Tetradecyloxy)-2-furoic acid, was administered at different times postinfection. Strikingly, the number of Tmem was only reduced when FAS was inhibited during T cell priming, but not during the Tmem survival phase. FAS inhibition during priming increased effector T cells (Teff) proliferation, and strongly decreased peak parasitemia, which is consistent with improved Teff function. Conversely, MPEC were decreased, in a T cell-intrinsic manner, upon early FAS inhibition in chronic, but not acute, infection. Early cure of infection also increased mitochondrial volume in Tmem compared to Teff, supporting previous reports in acute infection. We demonstrate that the MPEC-specific effect was due to the higher fatty acid content and synthesis in MPEC compared to terminally differentiated Teff. In conclusion, FAS in CD4 T cells regulates the early divergence of Tmem from Teff in chronic infection.

overall_design: B5 TCR Tg mice were infected with P. chabaudi. Effector and memory T cells subsets were sorted at day 8 and d60 post infection respectively. Naïve T cells from uninfected mice were sorted as well. Gene expression was measured in three effector subsets, three memory subsets and  and naive T cells. Two replicates were performed using different donors for each experiment.

first: Samad

last: Ibitokou

first: Brian

last: Dillon

first: Mala

last: Sinha

first: Bartosz

last: Szczesny

first: Anahi

last: Delgadillo

first: Doaa

last: Reda Abdelrahman

first: Csaba

last: Szabo

first: Lutfi

last: Abu-Elheiga

first: Craig

last: Porter

first: Demidmaa

last: Tuvdendorj


title: The funtion of DCLK1 in PNET cell

city: Kurume

first: Yu

last: Ikezono

state: Fukuoka

address: 67 Asahimachi

department: Department of Medicine

institute: Kurume University School of Medicine

summary: Comparison of the gene expression in DCLK1 overexpression cell and control cell

overall_design: Comparison of the gene expression in QGP1 (pancreatic neuroendocrine tumor (PNET) cells) transfected with empty vector and DCLK1 cDNA.

first: Hironori

last: Koga


title: Forced Expression of MIST1 in Parietal Cells

status: Public on Nov 01 2016

city: Houston.

first: Jason

last: Mills

state: T

address: One Baylor Plaza

department: Gastroenterology, Medicine

institute: Baylor College of Medicine

summary: MIST1 over-expression has not been analyzed in a cell type that does not express endogenous MIST1.  Here, we force-express ectopic MIST1 in the parietal cells of mouse stomachs.  We extracted whole corpus stomach mRNA and compared gene expression levels between MIST1-expressing mouse stomachs to controls.

overall_design: One stomach from each condition (MIST1-expressing and control) was taken from mice 12 weeks old for RNA extraction and hybridization on Affymetrix microarrays.  Whole stomachs were used.

first: Hei-Yong

middle: G

last: Lo


title: Impact of Sphingosine Kinase-1 knock out in neonatal mice lungs

status: Public on Oct 30 2016

city: Chicago

first: Zarema

last: Arbieva

state: IL

address: 835 S. Wolcott A301

department: RRC

institute: UIC

summary:
Sphingosine Kinase-1 knock out protects against hyperoxic lung injury
One day old Wild type (WT) control and Sphingosine Kinase-1 knock out  (SphK-1 KO)pups exposed to room air (RA) or hyperoxia (HO). Microarray based profiling of lung tissue after 7 days of hyperoxia of 75%

overall_design: WT RA, WT HO, SphK-1 KO RA, and Sph K-1 KO HO studied in triplicates

first: Anantha

last: Harijith

first: Alison

last: Ha

first: Yangbasai

last: Dong

first: Narsa

last: Machireddy

first: David

last: Ebenezer

first: J

middle: U

last: Raj

first: Sekhar

last: Pothireddy

first: Prasad

last: Kanteti

first: Mark

last: Maienschein-Cline

first: Vishwanathan

last: Natarajan


title: GABAA receptors and mother-derived taurine regulate neural progenitor cells specification in the mouse developing cortex

city: Toyohashi

first: Toshio

last: Kojima

address: 1-1 Hibarigaoka Tenpaku-cho

department: Health Care Center

institute: Toyohashi University of Technology

summary: The precise temporal regulation of the cellular properties of neural progenitor cells (NPCs) is essential for the histogenesis of the cerebral cortex. Neuroepithelial cells, the primary NPCs, transit to radial glia with astroglial properties. To coincide with this transition, NPCs start to differentiate into neurons, undergoing a switch from symmetric to asymmetric cell division. After the onset of neurogenesis, NPCs produce layer-specific neurons in a defined order. Here, we show that GABAA receptors and taurine are involved in this regulatory mechanism. Fetal exposure to GABAA blockers suppressed the transition to radial glia, the switch to asymmetric division and the differentiation into upper-layer neurons. Fetal exposure to GABAA positive modulators caused the opposite effects. Ca2+ imaging studies showed that NPCs principally responded to taurine, but not GABA, which is derived principally from mothers, before E13 via picrotoxin-sensitive receptors. Fetal exposure to GABAA receptor modulators resulted in considerable alterations in offspring behavior.

overall_design: All animal manipulations were performed in accordance with the National Institute of Health Guide for the Care and Use of Laboratory animals 8th ed. revised 2011 and were approved by the Animal Research Committee of University of Fukui and Animal Care and Use Committee at the University of Tokushima. Care was taken to minimize the numbers, pain and suffering of animals throughout the experiments. Embryonic stages were calculated with the day of the vaginal plug detection as embryonic day 0 (E0). Timed-pregnant C57BL/6N mice (SLC Japan) received two intraperitoneal (i.p.) injections of either saline (control) or 8 mg/mL phenobarbital in saline (80 mg/kg ) twice a day, 6 h apart on E10-11. Embryos were removed from the pregnant mice that were sacrificed by cervical dislocation at E12.

first: Shiro

last: Tochitani

first: Tomonori

last: Furukawa

first: Ryo

last: Bando

first: Shigeaki

last: Kondo

first: Takashi

last: Ito

first: Yoshitaka

last: Matsushima

first: Hideo

last: Matsuzaki

first: Atsuo

last: Fukuda


title: Exogenous expression of Lox, Loxl1 and Loxl2 regulate gene expression in primary murine lung fibroblasts.

status: Public on Oct 25 2016

city: Bad Nauheim

first: Rory

last: Morty

address: Parkstr. 1

department: W.G. Kerckhoff-Institut

institute: MPI für Herz- und Lungenforschung

summary: Primary murine lung fibroblasts were transfected with either control (scrambled) or sequence-specific siRNA against Lysyl oxidase (Lox), Lysyl oxidase-like (Loxl1) or Lysyl oxidase-like 2 (Loxl2) genes. Cells were harvested 48 hours after the transfection. Multiple changes in gene expression were found in the corrected p values in this microarray study.

overall_design: Four control (scrambled), four siLox, four siLoxl1 and four siLoxl2 transfected samples were used for this microarray study.

first: Ivana

last: Mižíková


title: Exogenous BAPN administration does not regulate gene expression in primary murine lung fibroblasts and alveolar epithelial type II (ATII) cells.

summary: Primary murine lung fibroblasts or ATII cells were either treated with vehicle or 1mM BAPN for 24 h. Overall, only one change in gene expression was found in the corrected p values in fibroblasts group in this microarray study.

overall_design: Four vehicle treated samples after 24 h of exposure and four BAPN treated (1mM) samples after 24 h of exposure, were used for this microarray study.


title: Gene array data from LOX p0 Mouse pups

status: Public on Oct 28 2016

city: St. Louis

first: Jessica

last: Wagenseil

address: One Brookings Dr.

department: Mechanical Engineering and Materials Science

institute: Washington Univeristy

summary:
Lysyl oxidase is an extracellular enzyme essential for crosslinking elastin and collagen. Mice that do not express Lox have 60% and 40% reductions in elastin-specific and collagen-specific crosslinks, respectively. Mutations in LOX are associated with thoracic aortic aneurysm and dissection (TAAD). Lysyl oxidase knockout mice dye perinatally with ruptured diaphragm, tortuous arteries, and TAAD
This is the first study to analyze the mechanical and genetic changes induced by the absence of lysyl oxidase in the thoracic aorta, and may provide new therapeutic targets relevant for the pathogenesis of thoracic aortic aneurysms and dissections

overall_design: For each sample, ascending and descending aortas from wild type and knockout p0 mouse pups were isolated, pooled in groups of eight, homogenized to isolate RNA, and processed for microarray analysis to identify genes with significantly changed expression between genotypes and/or anatomic location

first: Marius

last: Staiculescu


title: Prolonged intra-neutrophil survival as an adaptive strategy of Staphylococcus aureus USA300 to the hospital environment

status: Public on Nov 02 2016

city: Groningen

first: Jan Maarten

last: van Dijl

address: Hanzeplein 1

country: Netherlands

institute: University Medical Groningen

type: Expression profiling by high throughput sequencing

summary: Methicillin-resistant Staphylococcus aureus (MRSA) is the causative agent of serious hospital- and community-associated infections. Due to the global rise in community-associated MRSA, the respective lineages are increasingly introduced into hospitals. This raises the question whether and, if so, how they adapt to this new environment. The present study was aimed at investigating how MRSA isolates of the USA300 lineage, infamous for causing infections in the general population, have adapted to the hospital environment. To this end, a collection of community- and hospital-associated USA300 isolates was compared by RNA-sequencing. Here we report that merely 460 genes were differentially expressed between these two epidemiologically distinct groups, including genes for virulence factors, oxidative stress responses and the purine, pyrimidine and fatty acid biosynthetic pathways. Differentially regulated virulence factors included leukotoxins and phenol-soluble modulins, implicated in staphylococcal escape from immune cells. We therefore investigated the ability of the studied isolates to survive internalization by human neutrophils. This showed that the community-associated isolates have the highest neutrophil-killing activity, while the hospital-associated isolates are better adapted to intra-neutrophil survival. Importantly, the latter trait protects internalized staphylococci against a challenge with antibiotics. We therefore conclude that prolonged intra-neutrophil survival serves as a relatively simple early adaptation of S. aureus USA300 to the hospital environment where antibiotic pressure is high.

sample_organism: Staphylococcus aureus subsp. aureus USA300

overall_design: 12 bacterial isolates were grown in duplicate.  Samples were collected for RNA isolation from each replicates both from exponentially and stationary growing cells resulting in a total of 24 samples.

first: Solomon

last: Mekonnen

first: Eleni

last: Tsompanidou

first: Anne

last: de Jong

first: Tomasz

middle: K

last: Prajsnar

first: Annemarie

last: Meijer

first: Anders

middle: R

last: Larsen

first: Henrik

last: Westh

first: Alexander

last: Reder

first: Ulrike

last: Mäder

middle: W

last: Friedrich

first: Uwe

last: Völker


title: Gene expression profiles for human bone marrow-mesenchymal stromal cells (hBM-MSCs)

status: Public on Oct 18 2016

city: Seoul

first: Jung Min

last: Kim

address: Gangnam-gu Teheran-ro 216

department: Department of Health Genomics

country: South Korea

institute: NAR Center, Inc. & Genoplan, Inc.

summary: To compare the gene expression profile of hBM-MSCs at early (P3), late-passage (P7), and UBC gene knockdown (KD) from three different donors, we performed one-color microarray-based gene expression analysis.

overall_design: hBM-MSCs from three different donors: passage-3, passage-7, and UBC knockdown

first: Jiyeon

first: Yonggoo

first: Hayoung

last: Choi

first: Ahlm

last: Kwon

first: Jung

first: Myungshin


title: Gene expression analysis of mESCs following short-term inhibition with PD032, CHIRON, EPZ6438 and GSK-J4 both individually and in combination.

status: Public on Oct 11 2016

city: Edinburgh

first: Rob

last: Illingworth

state: Midlothian

address: Centre for Regenerative Medicine

department: Centre for regenerative Medicine

country: United Kingdom

institute: The University of Edinburgh

summary: This experiment was designed to determine the extent of gene misregulation in mouse ESCs cultured for 24hrs in different base medias and treated with the indicated inhibitors.

overall_design: Polyadenylated mRNA from mESCs cultured in the indicated culture conditions was hybridised as three independed biological replicates to Agilent SurePrint G3 Mouse GE 8x60K Microarrays (GPL10787). Individual replicates for each of the specified conditions were performed in HV H2b-mCh, HV9.3 and HFHC12.3 cell lines.

first: Robert

first: Jurriaan

middle: J

last: Hölzenspies

first: Fabian

middle: V

last: Roske

first: Josh

last: Brickman

first: Wendy

last: Bickmore


title: Gene expression analysis of enSLiT KO cells against Salmonella infection

status: Public on Oct 08 2016

city: Tokyo

first: Yayoi

last: Fukuoka

address: Hachioji Takakuracho

institute: Agilent

summary:
Eukaryotic genomes are pervasively transcribed, resulting in the production of many unstable nuclear long noncoding RNAs such as nuclear Short-Lived noncoding Transcripts (nSLiTs). However, the biological significance and turnover mechanism of nSLiTs are largely unknown.
We used microarrays to detail the global program of gene expression that is regulated by enSLiT upon Salmonella infection

overall_design: To assess the role of enSLiT against Salmonella infection, we knockout enSLiT07573 by using CRISPR/Cas9.  KO was performed replicate for each transcripts.  We comparied Salmonella infected/not infected HeLa cells and KO cells.  All data was obtained biological triplicate.

first: Katustoshi

last: Imamura

first: Nobuyoshi

last: Akimitsu


title: Whole genome gene expression profiles of H1299-shNaa10 and H1299-shRNA negative control

status: Public on Oct 07 2016

city: Hangzhou

first: Yong

last: Han

address: #158 Shangtang Road

institute: Zhejiang Provincial People's Hospital

first: Huiyu

last: Xu

first: Rong

last: Li


title: Gene expression analysis of LinSLiT08211 KO cells against Salmonella infection

summary:
Eukaryotic genomes are pervasively transcribed, resulting in the production of many unstable nuclear long noncoding RNAs such as nuclear Short-Lived noncoding Transcripts (nSLiTs). However, the biological significance and turnover mechanism of nSLiTs are largely unknown.
We used microarrays to detail the global program of gene expression that is regulated by LinSLiT08211 upon Salmonella infection

overall_design: To assess the role of LinSLiT against Salmonella infection, we knockout LinSLiT08211 by using CRISPR/Cas9.  KO was performed replicate for each transcripts.  We comparied Salmonella infected/not infected HeLa cells and KO cells.  All data was obtained biological triplicate.


title: AP-1 and TEAD4 co-operatively promote the vascular program during hemangioblast specification [expression]

status: Public on Oct 21 2016

city: Freiburg

first: Pierre

middle: Daniel

last: Cauchy

state: Baden-Württemberg

address: Breisacher Str. 115

department: Zentrum für Translationale Zellforschung

institute: University Medical Center Freiburg

summary: Embryonic blood cell development occurs via well-defined developmental stages which are recapitulated in vitro by differentiation of embryonic stem cells. This process is tightly regulated by the interaction of tissue- specific and ubiquitous transcription factors with the chromatin landscape in response to outside signals. We previously identified binding motifs for the commonly expressed AP-1 transcription factor family in open chromatin regions specific for early stages of blood specification and thus aimed to study the role of AP-1 for hemangioblast differentiation. Here we show that FOS and JUN together bind to and activate a core set of vascular genes in the hemogenic endothelium and that upon global inhibition of AP-1 by expression of a dominant negative FOS peptide the balance between endothelial and hematopoietic fate is shifted towards blood. Moreover, we demonstrate that in the hemogenic endothelium AP-1 is required for de novo binding of TEAD4, a transcription factor connected to Hippo signaling, to vascular genes. Notably, after the endothelial-to-hematopoietic transition TEAD4 binding is no longer persisting. These findings provide novel mechanistic insights into vascular and hematopoietic development.

overall_design: Gene expression patterns in developing hemogenic and hematopoietic cells with and without AP-1

first: Nadine

last: Obier

first: Salam

last: Assi

first: Jane

last: Gilmour

first: Michael

last: Lie-A-Ling

first: Maarten

last: Hoogenkamp

first: Monika

last: Lichtinger

first: Laura

last: Noailles

first: Peter

last: Cockerill

first: Georges

last: Lacaud

first: Valerie

last: Kouskoff

first: Constanze

last: Bonifer


title: A hypoxic signature marks tumors formed by disseminated tumor cells in the Balb-neuT breast cancer model

status: Public on Dec 01 2016

city: Torino

first: Raffaele

last: Calogero

state: To

address: Via Nizza 52

department: Molecular Biotechnology Center

country: Italy

institute: University of Torino

summary: Metastasis is considered to be the final and fatal stage of cancer progression. However, some evidence seems to indicate that tumor cell dissemination could occur early in the natural history of cancer progression. Early disseminated tumor cells (DTC) have been described in the bone marrow (BM) of patients suffering from diverse types of solid tumors as well as in experimental models.  The presence of early DTC - which share many features of dormant tumor cells - was found to correlate with later development of metastasis in several cancer types. However, little is known about the tumorigenic features of DTC obtained at different time points along tumor progression. Here, we investigated the actual tumorigenic capacities of DTC. We found that early DTC obtained from BM of 15-17 week-old Her2-neu transgenic (BALB-neuT) mice were not tumorigenic in immunodeficient mice.  In contrast, DTC-derived tumors were easily obtained (44 % frequency) when DTC from 19-22 week-old BALB-neuT mice (late DTC) were injected. Angiogenesis, which can contribute to regulate tumor dormancy in other systems, appeared dispensable to reactivate late DTC, although it accelerated growth of secondary DTC tumors. Gene expression profiling disclosed a distinctive transcriptional signature of late DTC tumors compared with that of mammary tumors, which was enriched for hypoxia-related transcripts and appeared to be maintained in cell culture ex-vivo. Immunohistochemical analysis confirmed high HIF-1α expression in DTC tumors, which was maintained in tumor-derived in vitro cultures. Altogether, these findings highlight a different tumorigenic potential of early and late DTC in the BALB-neuT model and describe a HIF-1α-related transcriptional signature in DTC tumors, which may render DTC angiogenesis-competent, when placed in a favourable environment.

overall_design: Four tumors derived from Early disseminated tumor cells (DTC) against four mammary tumors

first: Aichi

last: Msaki

first: Anna

last: Pasto

first: Matteo

last: Curtarello

first: Maddalena

last: Arigoni

first: Giuseppina

last: Barutello

first: Marco

last: Macagno

first: Federica

last: Cavallo

first: Alberto

last: Amadori

first: Stefano

last: Indraccolo


title: Acute p53 knock-out in mouse liver

city: Graz

first: Andreas

last: Prokesch

state: Styria

address: Harrachgasse 21/7

department: Institute of Cell Biology, Histology, and Embryology

country: Austria

institute: Medical University Graz

summary: Here we investigated the effects of acute p53 deletion on the fasting response in mice.

overall_design: p53 was depleted using p53 fl/fl mice with Adeno-Cre injection. Adeno-GFP was used as control. Before sacrificing, mice were fasted for 24 hours or fed ad-libitum.

first: Franziska

last: Graef

first: Miriam

last: Knauer

first: Matthias

last: Muenzer

first: Tim

last: Schulz

first: Michael

last: Schupp


title: Cocaine and shock labeled ribosome from mPFC

status: Public on Oct 01 2016

city: PALO ALTO

first: Li

last: Ye

state: California

address: 1050 Arastradero Rd Bulding B

institute: Stanford University

summary:
Activity-dependent ribosome profiling from mouse mPFC.
Ribosome from cocaine and shock activated cells were immunoprecipitated using antibody. Translating mRNA was isolated and analyzed.

overall_design: Ribosome TRAP mice were crossed to a ArcCre transgenic line. Activity-dependent ribosome labeling was enabled by subjecting mice to cocaine or shock in the presence of tamoxifen. Ribosome was genetically tagged with GFP in the activated cells and could be purified by immunoprecipitation.

first: Karl

last: Deisseroth


title: IL-23 promotes immunopathology and prevents IL-13-dependent tissue repair by Ly6Clo monocytes in parasite-induced liver damage

status: Public on Oct 03 2016

city: Hamburg

first: Thomas

last: Streichert

address: Martinistr. 52, Campus Forschung N27, 2. OG

department: Institute For Clinical Chemistry / Central Laboratories

institute: University Medical Center Hamburg-Eppendorf

summary: Background & Aims: The IL-23/IL-17 axis plays an important role in the pathogenesis of autoimmune diseases and the pathological consequences of infection. We previously showed that immunopathologic mechanisms mediated by inflammatory monocytes underlie the severe focal liver damage induced by the protozoan parasite, Entamoeba histolytica. Here, we analyze the contribution of the IL-23/IL-17 axis to the induction and subsequent recovery from parasite-induced liver damage. Methods: IL-23p19-/-, IL-17A/F-/-, CCR2-/-, and WT mice were intra-hepatically infected with E. histolytica trophozoites and disease onset and recovery were analyzed by magnetic resonance imaging. The expression of liver-specific genes and proteins during infection was examined by qPCR, microarray, FACS analysis and immunohistochemistry. Immuno-depletion and substitution experiments were performed in IL-23p19-/- and WT mice to investigate the role of IL-13 in disease outcome.  Results: Liver damage in infected IL-23p19-/-, IL-17A/F-/-, CCR2-/- mice was strongly attenuated compared with that in WT mice. IL-23p19-/- mice showed reduced expression of IL-17 and CCL2 genes and proteins. Increased numbers of IL-13-producing CD11b+Ly6Clo regenerative monocytes were associated with disease attenuation in IL-23p19-/- mice. Immuno-depletion of IL-13 in IL-23-/- mice reversed this attenuation and treatment of infected WT mice with an IL-13/anti-IL-13-mAb complex supported liver recovery.  Conclusions: The IL-23/IL-17 axis plays a critical role in the immunopathology of hepatic amebiasis. IL- 13 secreted by CD11b+Ly6Clo monocytes supports recovery from liver damage. An IL-13/anti-IL13- mAb complex mimics this function, suggesting a novel therapeutic option to support tissue healing after liver damage.

overall_design: Total liver RNA was extracted from wildtype and IL23-p19-/- mice previously infected intra-hepatically with E. histolytica trophozoites. The material was isolated 0 hours or 6 hours post infection.

first: Jill

last: Noll

first: Hanna

last: Lotter

first: Benjamin

last: Otto


title: Mouse lung tissue expression data after exposure to Cd-enriched water.

city: Atlanta

first: Joshua

last: Chandler

address: 615 Michael St

institute: Emory University

summary: Mice received 10 mg/L Cd in drinking water for 20 weeks, or normal water. At time of sacrifice, the lung tissue was harvested and RNA was extracted.

overall_design: 3 control and 3 Cd-treated are compared after RMA table generation with package 'oligo' followed by 'limma' for univariate analysis.

middle: D

first: Dean

middle: P

last: Jones


title: Effect of SUB1 knockdown on aggressive prostate cancer

city: Birmingham

first: Sooryanarayana

last: Varambally

state: Alabama

address: 1824 6th Avenue S

institute: University of Alabama

summary:
SUB1 is known to be playing critical role in vital cellular processes such as DNA replication, repair and heterochromatization. Expression profiling studies in several cancers show its overexpression. However, its regulation and function in cancer has been less explored.
Our study has indicated high expression of SUB1 in aggressive prostate cancer, we also found that the knockdown of SUB1 led to alterations in cell proliferation, invasion and migration. In addition, we found that mir-101, a tumor suppressor microRNA targets and regulates the expression of SUB1

overall_design: Two-color experiment.

first: B

last: Chakravarthi

first: S


title: Differential paralog divergence  modulates evolutionary outcomes in yeast

status: Public on Sep 30 2016

city: Seattle

first: Maitreya

middle: J.

last: Dunham

state: WA

address: Foege Building, S403B, Box 355065

department: Genome Sciences

institute: University of Washington

type: Genome variation profiling by genome tiling array

summary: Evolutionary outcomes depend not only on the selective forces acting upon a species, but also on the genetic background.  However, large timescales and uncertain historical selection pressures can make it difficult to discern such important background differences between species. Experimental evolution is one tool to compare evolutionary potential of known genotypes in a controlled environment.  Here we utilized a highly reproducible evolutionary adaptation in Saccharomyces cerevisiae to investigate whether experimental evolution of other yeast species would select for similar adaptive mutations.  We evolved populations of S. cerevisiae, S. paradoxus, S. mikatae, S. uvarum, and interspecific hybrids between S. uvarum and S. cerevisiae for 200-500 generations in sulfate-limited continuous culture.  Wild-type S. cerevisiae cultures invariably amplify the high affinity sulfate transporter gene, SUL1.  However, while amplification of the SUL1 locus was detected in S. paradoxus and S. mikatae populations, S. uvarum cultures instead selected for amplification of the paralog, SUL2.  We measured the relative fitness of strains bearing deletions and amplifications of both SUL genes from different species, confirming that, converse to S. cerevisiae, S. uvarum SUL2 contributes more to fitness in sulfate limitation than S. uvarum SUL1.  By measuring the fitness and gene expression of chimeric promoter-ORF constructs, we were able to delineate the cause of this differential fitness effect primarily to the promoter of S. uvarum SUL1.  Our data show evidence of differential sub-functionalization among the sulfur transporters across Saccharomyces species through recent changes in noncoding sequence.  Furthermore, these results show a clear example of how such background differences due to paralog divergence can drive changes in genome evolution.

sample_organism:
Saccharomyces bayanus
Saccharomyces cerevisiae

overall_design: All arrays are CGH comparing two genomes using two experimental designs.  Control experiments compare differentially labeled DNA from two species to test specificity.  The remaining experiments compare the genome content of an experimentally evolved strain with a control.

first: Aaron

last: Miller

first: Chris

last: Desevo


title: Gene expression profiles of Ecrg4-treated mouse microglia

status: Public on Sep 28 2016

city: Kobe

first: Kei

last: Enomoto

state: Hyogo

address: Chuo-ku, Minatojima-Minamimachi

institute: ASUBIO PHARMA CO., LTD.

summary: Esophageal cancer-related gene 4 (Ecrg4), a hormone-like peptide, is thought to be a tumor suppressor, however little is known about the mechanism of how Ecrg4 suppresses tumorigenesis. Using the mouse glioma–initiating cell models, we identified Ecrg4 acts as a tumor suppressor in vivo. To characterize the function of Ecrg4 towards microglia, an innate immune cell in central nervous system, we performed gene expression microarray analysis for primary microglia treated with or without recombinant Fc-fused Ecrg4 fragments. We demonstrate here that Ecrg4 fragments, amino acid residues 71-132 and 133-148, which are produced by the proteolitic cleavage, induced the expression of pro-inflammatory cytokines in microglia.  Thus, Ecrg4 acts as a cytokine/chemokine inducer, which activates the immune cells to eradicate tumor.

overall_design: Primary microglia cells from C57BL/6 mice were treated with PBS alone or 20 μg/ml of recombinant Fc, Fc-fused Ecrg4(71-132), or Fc-fused Ecrg4(133-148) for 3h. Duplicate for each assays were analyzed (8 samples in total).

first: Tetsuo

last: Moriguchi


title: Expression data from non-infected macrophages treated with conditioned medium from macrophages persistently infected with RSV virus

status: Public on Oct 15 2016

city: Mexico City

first: Ivan

last: Salido-Guadarrama

address: Calz. de Tlalpan 4502

country: Mexico

institute: Instituto Nacional de Enfermedades Respiratorias

summary: Persistent Respiratory syncytial virus (RSV) infection in humans, animal models and cell lines have proven persistence of viral genomic RNA and mRNA for long periods of time. Cell lines are well-established models that can be used to study alterations in the expression profile of the host genome. We postulate that RSV persistence might also indirectly induce changes in the homeostasis of non-infected cells through soluble factors. Thus, we evaluated the effect of conditioned medium (CM) from MΦP cultures on the transcriptional profile of non-infected macrophages through gene expression microarrays

overall_design: The persistently RSV infected macrophage-like cell line P388D1 (MΦP) was cultured during 24 and conditioned medium (CM-MΦP) was collected. Then, non-infected P388D1 macrophage-like cells (MΦN) were treated for 3 or 12 h with CM-MΦP or control-conditioned medium (CM-C) obtained from cultures of MΦN, passages 99 and 105.Total RNA was isolated and gene expression experiments were conducted per duplicate on the Affymetrix Mouse Gene 2.0 ST Array.

first: Evelyn

last: Rivera-Toledo

first: Mauricio

last: Rodríguez-Dorantes

first: Laura

last: Torres-González

first: Carlos

last: Santiago-Olivares

first: Beatriz

last: Gómez


title: Gene Expression data from synovium in mouse serum transfer arthritis model (STA) model

city: worcester

first: yukiko

last: maeda

state: massachusetts

address: 364 Plantation Street

department: Medicine

institute: Umass Medical School

summary:
To find regulated genes during peak inflammation of rheumatoid arthritis (RA), we have collected synovium from  mouse Serum Transfer Arthtitis (STA) model at day 0  (Non Arthritic) and day 10 (Peak Inflammation).
Serum transfer arthritis was induced in 12-week-old male C57BL/6J mice (The Jackson Laboratory) by intraperitoneal injection of 150 μl of arthritogenic serum on days 0, 2, and 7. Nonarthritic mice received 150 μl of sterile phosphate buffered saline at each time point.

overall_design: We analyzed gene expression data from Non-arthritic synovium pooled from 3 mice and Arthritic synovium at peak inflammation pooled from 10 mice. Two biological replicates for each time points.

first: Yukiko

last: Maeda

first: Nicholas

last: Farina

first: Melissa

last: Matzelle

first: Paul

last: Fanning

first: Jane

middle: B

last: Lian

first: Ellen

middle: M


title: Gene and miRNA Expression data from synovium in mouse serum transfer arthritis model (STA) model

type:
Expression profiling by array
Other

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: Development of gene expression signatures of murine silicosis in the lung CD45-negative tissue cells from CCR2 knockout mice

status: Public on Sep 24 2016

city: Chiba

first: Shigeyuki

last: Shichino

address: 2641, Yamasaki, Noda-shi

department: Department of Molecular regulation of Inflammatory and Immune Diseases

institute: Tokyo University of Science

summary:
Pulmonary fibrosis (PF) is an intractable disorder with a poor prognosis. Although macrophages are known to promote both the initiation and resolution of lung injury in reversible PF, it remains unclear how macrophages contribute to the progression of chronic PF. The object of this study was to investigate the role of inflammatory monocyte-derived macrophages (MMs) in the transcriptomic signatures of the lung tissue cells from murine progressive PF.
We collected CD45-negative lung tissue cells from silica-treated CCR2 knockout and WT mice on days 28, 40 and untreated mice on day 0 post-aspiration and performed global transcriptome analyses using microarray. Data were analyzed by fuzzy c-means or CLICK clustering, gene set enrichment analysis, and network analyses. Global transcriptome analyses revealed that MM deficiency potentiated changes in gene-expression in tissue cells, closely matching trends seen in human chronic PF. Regulatory network analysis of transcriptome data suggested that MM-derived factors, such as tumor necrosis factor-α, were involved in the suppression of tissue remodeling-related gene expression. Overall, these results demonstrate that MMs suppress tissue cell responses and associated pathology in progressive PF.

overall_design: Silica-induced gene expression in CD45-negative lung tissue cells from silica-treated CCR2 knockout and WT mice on days 28, 40 and untreated mice on day 0 post-aspiration was measured. Each total RNA sample pooled from 3 biological replicates (one experimental replicate) was analyzed using microarray.

first: Kouji

last: Matsushima

first: Mikiya

last: Otsuji

first: Satoshi

last: Ueha


title: Microarray analysis of white adipose tissue and liver from CD301b+ MNP-depleted mice

status: Public on Sep 22 2016

city: Newark

first: Yosuke

last: Kumamoto

state: NJ

address: 205 South Orange Ave

department: Center for Immunity and Inflammation

institute: Rutgers University

summary: Tissue-resident mononuclear phagocytes (MNPs) in metabolic organs contribute to the regulation of whole body metabolism. CD301b+ MNPs are a subset of MNPs that are found in most peripheral organs including metabolic organs.  In a mouse model in which CD301b+ MNPs can be selectively and transiently depleted, we examined the impact of the depletion on gene expression in the white adipose tissue and the liver.

overall_design: Male Mgl2-DTR mice or control wild-type mice were treated with diphtheria toxin for 10 days to depleted CD301b+ MNPs. Total RNA was isolated frrom the inguinal and epididymal white adipose tissue and the liver.

first: Akiko

last: Iwasaki


title: Embryonic sensory thalamus nuclei-specific genes revealed by genetic labelling and FACS isolation

status: Public on Sep 21 2016

city: San Juan de Alicante

first: Guillermina

last: López-Bendito

state: Alicante

address: Av. Ramón y Cajal, s/n

department: Developmental Neurobiology

country: Spain

institute: Instituto de Neurociencias de Alicante CSIC & UMH

summary:
To identify genes expressed in specific developing thalamic nuclei during embryonic stages, a genetic dual labelling strategy was established to mark and isolate the cells. Transcription profiles were determined for the principal sensory thalamic populations by genome-wide analysis.
We identified genes expressed in distinct thalamic nuclei with a potential function in the specification of individual sensory-modality thalamocortical connections.

overall_design: Thalamic neurons were isolated by FACS based on fluorescence intensity of dual genetic labeling by Gbx2CreER-IRES-EGFP/+::R26lsl-tdTomato/+. Array was made on total RNA from 3 biological replicates of 3 different populations (9 samples) taken at E18.5 and 3 biological replicates of 2 different populations (6 samples) taken at E14.5

first: Henrik

last: Gezelius


title: Bcl11a Deficiency Leads to Hematopoietic Stem Cell Defects with an Aging-like Phenotype

status: Public on Sep 20 2016

city: Boston

first: Jialiang

last: Huang

state: MA

address: 450 Brookline Avenue

institute: Dana-Farber Cancer Institute

summary: B cell CLL/lymphoma 11A (BCL11A) is a transcription factor and regulator of hemoglobin switching that has emerged as a promising therapeutic target for sickle cell disease and thalassemia. In the hematopoietic system, BCL11A is required for B lymphopoiesis, yet its role in other hematopoietic cells, especially hematopoietic stem cells (HSCs) remains elusive. The extensive expression of BCL11A in hematopoiesis implicates context-dependent roles, highlighting the importance of fully characterizing its function as part of ongoing efforts for stem cell therapy and regenerative medicine. Here, we demonstrate that BCL11A is indispensable for normal HSC function. Bcl11a deficiency results in HSC defects, typically observed in the aging hematopoietic system. We find that downregulation of cyclin-dependent kinase 6 (Cdk6), and the ensuing cell-cycle delay, correlate with HSC dysfunction. Our studies define a mechanism for BCL11A in regulation of HSC function and have important implications for the design of therapeutic approaches to targeting BCL11A.

overall_design: We crossed the Bcl11a floxed strain to the interferon-inducible Mx1-Cre mouse strain (Kühn et al., 1995) to evaluate the role of Bcl11a in postnatal hematopoiesis. From this cross we obtained non-deleted (WT; Bcl11afl/fl x Mx1-Cre–), heterozygously deleted (Het; Bcl11afl/wt x Mx1-Cre+) and homozygously deleted (KO; Bcl11afl/fl x Mx1-Cre+) animals. To induce Bcl11a gene deletion, mice were administered five injections of Polyinosinic:polycytidylic acid, p(I:C) (Figure 2A). Hematopoietic stem cells from WT, Het and KO mouse were selected for RNA extraction and hybridization on Affymetrix microarrays. Each group contains three biological replicates.

first: Sidinh

last: Luc


title: Diurnal transcriptome rhythms in mice with genetically ablated clock function in the suprachiasmatic nucleus (SCN)

city: Lübeck

last: Oster

address: Marie Curie Street

department: CBBM

institute: University of Lübeck

summary: Male KO (Syt10-Cre/Cre x Bmal1-flox/-) and CON (Syt10-Cre/Cre x Bmal1-+/-) mice were entrained to 12h:12h light:dark conditions for two weeks and sacrificed at 4 different time points (CT1, 7, 13, 19) on the second day after release into constant darkness conditions. Total RNA was isolated from epididymal white adipose tissue biopsies and subjected to microarray hybridization.

overall_design: 3 mice were used at each time point, for both CON and MUT groups

first: Isa

last: Kolbe

first: Jana

last: Husse

first: Gabriela

last: Salinas

first: Thomas

last: Lingner

first: Mariana

last: Astiz


title: Gene expression profiling from pooled samples of liver tissue of liver MyD88 WT mice and MyD88 liver specific KO mice fed either with a control diet or a high-fat diet.

status: Public on Sep 13 2016

city: Brussels

first: Jean-Baptiste

last: Demoulin

address: av Hippocrate 75, B1.74.05

department: de Duve Institute

country: Belgium

institute: Université catholique de Louvain

summary: Mice wild type or knocked-out for the MyD88 gene specifically in liver, were recruited for this expression profiling experiment. Each group of mice (WT versus LKO) were fed with a control diet or a high fat diet. Then mice were sacrificed and liver samples form were processed for RNA extraction. Total liver RNA of each sample was then pooled with those of the same group and treatment for microarray hybridization.

overall_design: four groups of mice: (I) WT-CT, (II) MyD88 liver specific KO (LKO-CT), (III) WT treated with high-fat diet (WT-HFD) and (IV) MyD88 liver specific KO treated with high-fat diet (LKO-HFD) .

first: Thibault

last: Duparc

first: Amandine

last: Everard

first: Ahmed

last: Essaghir

first: Patrice

last: Cani


title: Exogenous remodeling of the lung macrophage microenvironment protects against infectious consequences of bone marrow ablative chemotherapy

status: Public on Sep 26 2016

city: Memphis

first: Geoffrey

last: Neale

state: TN

address: 262 Danny Thomas Place

department: Hartwell Center

institute: St Jude Childrens Research Hospital

summary: Infection is the single greatest threat to survival during cancer chemotherapy because of depletion of bone marrow derived immune cells. In the absence of phagocytes such as neutrophil, vaccine-induced humoral and cellular anti-pathogen immunity are compromised. Using a model of vaccine-induced protection against lethal P. aeruginosa pneumonia in the setting of chemotherapy-induced neutropenia, we found a population of resident lung macrophages in the immunized lung that mediated protection in the absence of neutrophils, bone marrow derived monocytes, or antibodies. These vaccine-induced macrophages (ViMs) expanded after immunization, locally proliferated, and were closely related to alveolar macrophages (AMs) by surface phenotype and gene expression profiles. By contrast to AMs, numbers of ViMs were stable through chemotherapy, show enhanced phagocytic activity, and prolonged survival of neutropenic mice from lethal P. aeruginosa pneumonia upon intratracheal adoptive transfer. Thus, induction of ViMs by tissue macrophage remodeling may become a framework for new strategies to activate immune-mediated reserves against infection in immunocompromised hosts.

overall_design: We compared the global transcription profiles of three different populations of resident lung macrophages in mice following intranasal immunization with a live-attenuated Pseudomonas aeruginosa vaccine (strain PAO1ΔaroA) with or without cyclophosphamide (CY) treatment. Macrophages were isolated from collagenase-digested whole lung at 4 weeks after 3 weekly doses of immunization with or without CY (150mg/kg/dose i.p.) on days -6, -4, -2 of harvest.  Overall, there were three treatment groups: Control (unvaccinated, no CY treatment), Vac only (vaccinated but not treated with CY), or Vac+CY (vaccinated and CY-treated). Five mice from each treatment group were pooled and treated as a single sample for microarray analysis to guarantee enough number of cells for each assay. Each treatment group consisted of biologically independent triplicates which were processed in 3 independent experiments.

first: Akinobu

last: Kamei

first: Geli

last: Gao

first: Lip

middle: N

last: Loh

first: Peter

last: Vogel

first: Paul

last: Thomas

first: Elaine

middle: I

last: Tuomanen

last: Murray


title: Gene expressions regulated by N/C interacting and non-interactiong GR

city: RTP

first: NIEHS

last: Microarray Core

state: NC

address: 111 T.W. Alexander Drive

department: DIR

institute: NIEHS

summary: Glucocorticoid receptor (GR) was demonstrated to undergo an N/C interaction between the 26VMDFY30 motif in the N-terminus and C-terminal LBD in the presence of its co-chaperone cytoplasmic constitutive active/androstane receptor retention protein (CCRP). Utilizing the fact that phosphor-mimic mutation of tyrosine 30 to glutamic acid abolished this N/C interaction, CCRP and either GR Y30F or GR Y30E mutant was ectopically expressed in COS-1 cells for subsequent cDNA microarray analysis. Dexamethasone, a potent GR ligand, significantly induced or repressed 673 and 689 genes in Y30F and Y30E, respectively. Among them, only 166 genes were commonly regulated. This analysis strongly suggested that the GR N/C interaction serves to regulate distinct gene sets.

overall_design: Gene expressions induced by dexametahsone treatment for 6 hours were measured in COS-1 cells were transiently transfected with mCCRP-V5 and FLAG-hGR (Y30F or Y30E). Three repricates were used in each group. As negative controls, samples prepared from 0.1% DMSO treated cell were used.

first: Marumi

last: Ohno


title: Transcriptomic data to assess hexavalent chromium mode of action in mice and rats

city: Chapel Hill

first: Julia

last: Rager

address: 135 Dauer Drive, CB 7431

institute: UNC

sample_organism:
Mus musculus
Rattus norvegicus

platform_organism:
Mus musculus
Rattus norvegicus


title: Gene expression differences between wildtype and Atrx conditional knockout mouse retina tissues

status: Public on Sep 09 2016

city: Ottawa

first: Pamela

last: Lagali

state: Ontario

address: 501 Smyth Road

department: Regenerative Medicine Program

institute: Ottawa Hospital Research Institute

summary:
Loss of the Atrx chromatin remodeling protein causes dysfunction and death of post-mitotic retinal interneurons in mice. Embryonic conditional deletion of Atrx from multipotent retinal progenitor cells results in the selective loss of the retinal inhibitory interneurons, namely amacrine and horizontal cells. The cell death occurs postnatally after the development of these cell types, peaking at postntal day 17 in the mouse retina.  Identification of molecular factors and pathways that mediate the health and survival of these neurons may suggest novel therapeutic strategies for neuroprotection in ATR-X syndrome and other neurodegenerative diseases.
We performed gene expression profiling of wildtype and Atrx conditional knockout mouse retina tissues to identify putative targets of Atrx and molecular pathways that underlie the neurodegenerative phenotype.

overall_design: Mouse retinas were isolated from Chx10Cre-mediated Atrx cKO and wildtype (Cre-) littermates at postnatal day 17 (P17) for RNA extraction and hybridization to Affymetrix mouse gene microarrays. P17 is the age at which the peak of retinal amacrine and horizontal cell neurodegeneration is reached in the Atrx cKO mice.

middle: S

first: David

last: Picketts


title: Effect of MLL3 deletion in mammary stem cells

status: Public on Sep 19 2016

city: New York

first: Wenjun

last: Guo

state: NY

address: 1301 Morris Park

department: Cell Biology

institute: Albert Einstein College of Medicine

summary:
MLL3 inactivation mutations occurs frequently in human breast cancer. To understand the function of MLL3 inactivation, we compared the gene expression profiles of the vector control (WT)
and Mll3-null mouse mammary stem cells generated by CRISPR. Affymetrix mouse Gene 2.0ST ships were used for microarray.

overall_design: Mammary stem cell lines were generated by CRISPR. Total RNA was extracted from stem cells cultured as organoids and used for microarray analysis.

first: Zheng

last: Zhang


title: Common pathways involved in adipose tissue inflammation and atherosclerosis

status: Public on Sep 01 2016

city: Vienna

first: Thomas

last: Stulnig

address: Waehringer Guertel 18-20

department: Christian Doppler Laboratory for Cardio-Metabolic Immunotherapy and Clinical Division of Endocrinology and Metabolism, Department of Medicine III

institute: Medical University of Vienna

summary: Adipose tissue inflammation and atherosclerosis are the main mechanisms behind type 2 diabetes and cardiovascular disease respectively, the major risks associated with the metabolic syndrome. Studies considering more than single factors behind the complexity of the metabolic syndrome are valuable to achieve a better and wider understanding of the metabolic syndrome. In this study common dysregulated pathways between adipose tissue inflammation and atherosclerosis were identified using two different bioinformatic tools to perform pathway analysis. First, we run a gene set enrichment analysis utilizing with data from two microarray experiments done with gonadal white adipose tissue and atherosclerotic aorta. Once the common dysregulated pathways between both tissues were identify, the inflammatory response and the oxidative phosphorylation pathways from the Hallmark geneset were selected to conduct a deeper checkup at the single gene level of these pathways. Second, we carried out a pathway analysis validation with the Panther™ software combining the microarray data with a published type 2 diabetes mellitus metanalysis and cardiovascular disease metanalysis which included human data. In conclusion, this study provides worthwhile data pointing out and describing several dysregulated and common pathways in adipose tissue inflammation and atherosclerotic aorta with a potential implication in the pathogenesis of type 2 diabetes and atherosclerosis.

overall_design: LDLR-/- on a C57BL/6J background, purchased from Charles River Laboratories (Sulzfeld, Germany) were used. At 9 weeks of age the LDLR-/- were placed for up to 20 weeks on sucrose-enriched high-fat diet (HFSC) (with 17.5 kcal% from sucrose; (D09071704, Research Diets Inc.). Their respective controls were kept on normal chow diet (NC) for up to 20 weeks. After sacrificing the gonadal white adipose tissue (GWAT) from  LDLR-/- animals on NC (Samples 22-27) or HFSC (Samples 28-33)  was collected as well as the whole aortae from LDLR-/- animals on  NC (Samples 13-15) or HFSC (Samples16-18). The collected tissues were immediately snap frozen in liquid nitrogen. RNA was isolated for gene expression microarray analyses at the exon level (GeneChip Mouse Exon 2.0 ST Array, Affymetrix, Santa Clara, CA, USA). To isolate RNA, the frozen tissue samples were homogenized in TRIzol® reagent (Invitrogen/Life Technologies, Carlsbad, CA, USA) and processed based on manufacturer’s instructions. Total RNA (1μg) was then used for GeneChip analysis, individual samples were used in GWAT preparation and three samples were pooled and used for aorta preparations. Terminal-labeled cDNA, hybridization to genome-wide Mouse Gene 2.0 ST Gene Chips and scanning of the arrays were carried out according to the manufacture’s indications (Affymetrix).Output primary row data was analyzed with Expression Console software (Affymetrix).

first: V

last: Moreno-Viedma

first: M

last: Amor

first: A

last: Sarabi

last: Jeitler

last: Bilban

first: K

last: Kodama

last: Butte

first: G

last: Staffler

last: Zeyda

first: T


title: Human Gastric Cancer Cell line MKN45: Non-Target shRNA vs. SET/I2PP2A targeting shRNA

status: Public on Sep 06 2016

city: Yamaguchi

first: Takashi

last: Ohama

address: 1677-1 Yoshida

institute: Yamaguchi University

summary: Transcriptional profiling of MKN45 cells comparing control stably expressing Non-Targeting shRNA  cells with stably expressing SET/I2PP2A targeting shRNA cells. Goal was to determine the effects of SET knockdown on MKN45 gene expression.

overall_design: Comparison between stably expresing cells: Non-Targeting shRNA vs. SET/I2PP2A shRNA cells.


title: Role of Dicer1-dependent microRNAs in the paracrine control of epididymal gene expression

city: Quebec

first: Ezequiel

middle: L

last: Calvo

state: Quebec

address: 2705 Boul. Laurier

department: Molecular Endocrinilogy

institute: CRCHUL

summary: Dicer1 is an endoribonuclease involved in the biogenesis of functional microRNAs (miRNAs). These small non-coding RNAs are important regulators of the posttranscriptional gene expression and participate to the control of male fertility. Knowing that 1) Dicer1-dependent factors are needed for proper sperm maturation in the epididymis, and that 2) miRNAs are potent mediators of intercellular communication in most biological systems, we investigated the role of Dicer1 dependent-miRNAs produced from the proximal epididymis (initial segment/caput) on the paracrine regulation of epididymal gene expression in the distal epididymis regions (i.e. corpus and cauda). To this aim, we performed comparative microarray and ANOVA analyses on control vs. Defb41iCre/wt;Dicer1fl/fl mice in which functional Dicer1 is absent from the principal cells of the proximal epididymis. We identified 21 and 16 transcripts, including Prostate And Testis Expressed 4 protein and the Zn-alpha 2-glycoprotein, that display significant expression level changes in the corpus and cauda regions, respectively (Fold change >2 or <-2; p<0.001). In addition, 154 miRNAs, including miR- 210, miR-672, miR-191 and miR-204, show a significantly impaired biogenesis in the absence of Dicer1 from the proximal epididymis (Fold change>2 or <-2; p<0.01). These miRNAs are secreted via extracellular vesicles derived from DC2 epididymal principal cell line, and their expression correlates with target transcripts involved in important biological pathways, as evidenced by in silico analysis. These observations suggest that Dicer1-dependent miRNAs could act as potent paracrine regulators of epididymal functions (i.e. control of sperm motility, ciliogenesis) and may contribute to the infertility phenotype observed in the Defb41iCre/wt;Dicer1fl/fl mouse model. These findings open new avenues for the identification of molecular targets important to male fertility control.

overall_design: Epididymides from Dicer1fl/fl (Control) and Defb41iCre/wt;Dicer1fl/fl (Dicer cKO) were used in this study. Total RNA was isolated from the initial segment/caput, the corpus and the cauda epididymal regions from 3 control and 3 Dicer1 cKO mice.

first: Clémence

last: Belleannée

first: Olivia

last: Jerczynski

first: Nicolas

last: Lacroix-Pépin

first: Eric

last: Boilard

first: Ézéquiel

first: Michel

last: Fortier

first: Ida

last: Björkgren

first: Petra

last: Sipilä


title: Gene expression analysis of mouse lymphatic endothelial cells (LECs) from the subcapsular sinus (SS, afferent) and lymphatic sinus (LS, efferent)

status: Public on Aug 24 2016

city: Turku

first: Kati

last: Elima

address: Tykistökatu 6

department: MediCity

country: Finland

institute: University of Turku

summary: Afferent lymphatic vessels bring antigens and diverse populations of leukocytes to draining lymph nodes, but efferent lymphatics allow only lymphocytes to leave the nodes. Despite fundamental importance of afferent vs. efferent lymphatics in immune response and cancer spread, molecular characteristics of these different arms of the lymphatic vasculature are largely unknown. In this work we report marked transcriptional differences between afferent and efferent lymphatic endothelial cells.

overall_design: Mouse inguinal, axillary, and brachial lymphnodes were collected and cryomolds prepared for laser-capture microdissection.  Frozen sections were stained with various cell marker antibodies and micro-dissection performed to collect lymphatic endothelial cells. Total RNA was extracted from the cells and used in microarray analysis. Alternatively, popliteal, caudal, lumbar, inguinal, mesenteric, renal, axillary, brachial, deep and superficial cervical LN were enzymatically digested, the cells stained, and FACs sorted before RNA isolation.

first: Imitiaz

last: Iftakhar-E-Khuda

first: Sirpa

last: Jalkanen

first: Marko

last: Salmi

first: Anu

last: Kukkonen-Macchi

first: Ruth

last: Fair-Mäkelä


title: Analysing gene expression signatures of whole thymospheres derived from adult (A) or embryonic day 14.5 (E) mouse thymus

status: Public on Sep 14 2016

city: Heidelberg

first: Olga

last: Ucar

address: Im Neuenheimer Feld 280

department: Developmental Immunology

institute: German Cancer Research Center

summary:
Thymosphere-forming cells undergo phenotypic changes during ontogeny that are likely to reflect changes in gene expression patterns within thymospheres. We therefore isolated total RNA from pooled thymospheres derived from E14.5 or adult thymic digests and analysed their transcriptome by whole-genome microarrays.
Several thymic epithelial markers including those associated with progenitor cells were differentially expressed in embryonic vs adult thymospheres. Gene ontology analysis revealed that pathways related to major key biological processes displayed changes between these two stages of ontogeny. We found significant differences in pathways involved in cell proliferation, development and differentiation, cell metabolism, regulation of transcription and regulation of DNA repair. Most interestingly, we observed significant enrichment of gene expression in several signalling pathways.

overall_design: Thymic digests were plated into ultra low attachment culture and thymospheres were allowed to grow for seven days. Grown thymospheres were collected on filters to wash off remaining single cells and immediately lysed in Trizol. Two independent biological and technical replicates were performed.

first: Bruno

last: Kyewski


title: Motor phenotypes and molecular networks associated with germline  deficiency of Ciz1

first: Satya

last: Vemula

address: 855 Monroe Avenue, Suite 415 Link Building

department: Neurology

institute: University of Tennessee Health Science Center

summary:
A Ciz1 gene-trap knock-out (KO) mouse model was generated to examine the functional role(s) of Ciz1 in the sensorimotor nervous system and contributions of Ciz1 to cell-cycle control in the mammalian brain.
Ciz1 transcripts were absent in Ciz1-/- mice and reduced by approximately 50% in Ciz1+/- mice

overall_design: Total RNA harvested from cerebellum of 6-10-month old Ciz1-/- and 6 age and gender matched WT mice were used for wholegenome gene expression analysis

first: Jianfeng

last: Xiao

first: Mark

last: LeDoux


title: Host response in cells from broncho-alveolar lavage (BAL) isolated from mice infected with influenza virus (PR8) and/or Staphylococcus aureus (Newman)

city: Seattle

first: Aderem

last: Lab

address: 307 Westlake Avenue North, Suite 500

institute: Seattle Children's Research Institute

summary: Array analysis of total RNA from broncho-alveolar lavage (BAL) from mice infected with influenza virus (PR8) and/or Staphylococcus aureus (Newman)

overall_design: Primary infection: mock or influenza virus (PR8) at 100 PFU on day 0 (intranasal); Secondary infection: mock or Staphylococcus aureus (Newman) at 1x10^8 CFU on day 7 (non-invasive intratracheal); Time point:  4 h post secondary infection

first: Vincent

middle: C

last: Tam

first: Alan

last: Aderem


title: Gene Expression Analysis Indicates Divergent Mechanisms in DEN-Induced Carcinogenesis in Wild Type and Bid-Deficient Livers

city: Indianapolis

first: Xiaoming

last: Yin

state: Indiana

address: 350 West 11th street

department: Department of Pathology and Laboratory Medicine

institute: Indiana University School of Medicine

summary:
The aim of this study was to better understand the Bid-regulated events during hepatic carcinogenesis.
The information from this set of data indicates that wild type and bid-deficient livers express different sets of genes after diethylnitrosamine (DEN) treatment.

overall_design: We performed gene expression analysis in wild type and bid-deficient mice treated with DEN for 4-6 months and for 10-12 months. The expression was compared among the different groups to understand the effect of deletion of Bid on gene epxression at the early (4-6 month) and the later (10-12 months) stage.

first: Changshun

last: Yu