title: Chd4 deficiency effect on mouse embryonic stem cells

status: Public on May 01 2017

first: Haixin

address: Yueyang Road 320

institute: Institute of Health Sciences, Shanghai Institutes of Biological Sciences, Chinese Academy of Sciences

summary:
Our study reveal that Chd4 is essential for stemness maintenance of ESCs. As Chd4 deficient ESCs show attentuated self-renewal ability and induced differentiation marker gene expression.
To confirm the effect of Chd4 on the transcriptome profile of ESCs, we performed microarray analyses for Chd4 deficient ESCs.

overall_design: We used the Tet-on inducible RNAi cell lines to achieve Chd4 knockdown. we performed microarray assays from 2 experimental groups with biological duplicate samples, Chd4i-1 cells treated with 5 ng/ml doxycyline for 3 days as the experimental group and without Dox treatment as the control group.

first: Ying

last: Jin


title: High-fat diet promotion of endometriosis in an immunocompetent mouse model is associated with altered peripheral and ectopic lesion redox and inflammatory status

status: Public on Apr 23 2017

city: Little Rock

first: Rosalia

middle: CM

last: Simmen

state: AR

address: 4301 West Markham  Mail Slot 750

department: Physiology and Biophysics

country: USA

institute: University of Arkansas for Medical Sciences

summary: Endometriosis is a benign gynecological condition that causes significant morbidity due to reduced fertility, pelvic pain and inflammatory dysfunctions. High-fat dietary intake has been linked to higher systemic inflammation and oxidative stress, which are both features of women with endometriosis. We evaluated the effects of high-fat diet (HFD) on endometriosis progression using immunocompetent mouse model wherein ectopic lesion was induced in wildtype and kruppel-like factor 9 (KLF9)- null donor mice. Results showed that HFD leads to increased ectopic lesion numbers and higher body weight gain. The HFD-promotion of lesion establishment was associated with decreased stromal estrogen receptor 1 and progesterone receptor expression, increased macrophage infiltration, and enhanced expression of pro-inflammarory and pro-oxidative stress pathway genes. Further, lesion-bearing mice had higher peritoneal fluid TNF-α and elevated local/systemic redox status than control-fed mice.

overall_design: Mice with endometriotic lesions fed high-fat diet or control diet.

first: Melissa

middle: E

last: Heard

first: Stepan

middle: B

last: Melnyk

first: Frank

middle: A

first: Yanqing

last: Yang

first: John

middle: M

last: Pabona

middle: C


title: Memory CD4 T cells help adaptive immunity with minimal immunopathology

status: Public on Mar 31 2017

city: Boston

first: MALIKA

last: AID

state: MA

address: 3 blackfan street

institute: BIDMC

summary:
CD4 T cells play critical roles in promoting inflammation and helping immune responses, but knowledge of how memory CD4 T cells are regulated and how they help adaptive immune responses is limited. Using adoptive transfer of virus-specific CD4 T cells, we show that naïve CD4 T cells undergo substantial expansion following viral infection, but can induce lethal TH1-driven inflammation. In contrast, memory CD4 T cells exhibit a biased proliferation of T follicular helper (Tfh) cell subsets that correlate with improved adaptive responses and minimal tissue damage following viral infection. Importantly, our analyses revealed that type I interferon regulates the expansion of naïve CD4 T cells, but does not seem to play a critical role in regulating the expansion of memory CD4 T cells. Moreover, blockade of type I interferon signaling abrogated lethal CD4 T cell inflammation following viral infection. Taken together, these data demonstrate a previously undescribed function for memory CD4 T cells: to help adaptive immunity with minimal harm to the host. These findings are important for rational vaccine design and for improving the safety and efficacy of adoptive T cell therapies against persistent antigens.
Primary and memory SMARTA cells were MACS-purified by negative selection (STEMCELL) and then FACS-sorted to 98% purity on a FACS Aria (BD Biosciences) according to congenic marker expression (CD45.1+ for secondary, and CD45.1+ CD45.2+ for primary, CD4 T cell responses).

overall_design: We explored the differences between secondary CD4 compared to Primary CD4.

first: Mitra

last: Bhatacharyya

first: Nathan

last: Henning

first: Malika

last: Aid

first: Amanda

last: Martinot

first: Dan

middle: H

last: Barouch

first: Pablo

last: Penaloza-MacMaster


title: Colon epithelial cells gene expression data of Sphingomyelin synthase 2 knockout colitis mice

city: Uchinada

first: Chieko

last: Hashizume

address: 1-1 Daigaku

department: Medicine

country: Japan

institute: Kanazawa Medical University

summary: Sphingomyelin synthase (SMS) 2 is the synthetic enzyme of sphingomyelin (SM), which regulates the fluidity and microdomain structure of the plasma membrane. We investigated the effect of SMS2 deficiency on dextran sodium sulfate (DSS)-induced murine colitis, and found suppression of DSS-induced inflammation in SMS2 deficient (SMS2-/-) mice. Results provide insight into the role of SMS2 in inflammation.

overall_design: Colon epithelial cells were isolated from wild-type (WT) and SMS2 knockout mice at day 2 after initiation of DSS treatment or untreated controls. Two independent biologic replicates were performed.

first: Toshio

last: Ohnishi

first: Toshiro

last: Okazaki


title: Genexpression of murine mesothelioma cell lines AC29 and AB1

status: Public on Mar 29 2017

city: Rotterdam

first: Floris

last: Dammeijer

address: Wytemaweg 80

department: Pulmonary Medicine

country: Netherlands

institute: Erasmus MC

summary: RNA from two murine mesothelioma cell lines (AC29 and AB1) was extracted and hybridized to Affymetrix Microarrays to compare gene expression. Both mesothelioma cell lines were established following intraperitoneal introduction of crocidolite (asbestos) fibers (Davis et al. 1992) in CBA mice (AC29 cell line), and BALB/c mice (AB1).

overall_design: AB1 (passage #40) and AC29 (passage #60) cell lines were cultured in 3 T75 flasks per cell line and were harvested at 80% confluency after RNA was extracted from each flask and hybridized to Affymetrix Microarrays.

first: M

last: Kaijen-Lambers

first: S

last: Swagemakers

first: F


title: Estrogen signaling and fatty liver disease

status: Public on Mar 22 2017

city: RTP

first: NIEHS

last: Microarray Core

state: NC

address: 111 T.W. Alexander Drive

department: DIR

institute: NIEHS

summary:
We propose comparing liver gene expression of WT and female ERKO mice early in the high-fat feeding period to animals fed a regular chow diet. Analyzing liver tissue before the fatty liver disease phenotype becomes severe will allow identification of target genes which may be causal.
Comparison of regular chow fed WT animals to high fat fed WT animals will allow for identification of hepatic genes up-regulated in response to high fat feeding. Comparison of regular chow fed WT animals to regular chow fed ERKO animals will help clarify hepatic gene expression patterns that may be implicated in increased susceptibility to weight gain and glucose intolerance. Comparison of high fat fed WT animals to high fat fed ERKO animals will provide insight into genes that could be implicated in leading to increased fat accumulation in the liver over time during high fat feeding. Finally, comparison of regular chow fed ERKO animals to high fat fed ERKO animals will help identify genes that may be contributing to increased liver fat accumulation in response to high fat feeding in these animals.

overall_design: The liver tissue was collected from high-fat diet fed and regular diet fed WT and aERKO females for RNA extraction and hybridization on Affymetrix microarrays.

first: Sarah

last: Hart-Unger

first: Kenneth

middle: S

last: Koach


title: Expression data from precancerous mouse liver under PI3K signaling activation with or without Kdm3a defficiency

status: Public on Apr 01 2017

city: Bunkyo-ku

first: Takuma

last: Nakatsuka

state: Tokyo

department: Gastroenterology

institute: The University of Tokyo

summary:
Epigenetic gene regulation in various oncogenic pathways is currently an important focus of cancer research. The PI3K pathway plays a pivotal role in hepatocellular carcinoma, but the significance of histone modification in the PI3K pathway-dependent hepatotumorigenesis remains unknown.
We used microarrays to investigate the oncogenic gene regulation by histone demethylase Kdm3a under PI3K signaling activation in the liver.

overall_design: We investigate the role of a histone demethylase KDM3A in liver tumor development by crossing the hepatocyte-specific Pik3ca transgenic mice and the Kdm3a knockout mice. We obtained the material specimen from precancerous liver tissue and analyze it.

first: Keisuke

last: Tateishi


title: RNA expression across 6 strains of mice in relation to prepulse inhibition testing, as described in: Pdxdc1 (pyridoxal-dependent decarboxylase domain containing 1) modulates pre-pulse inhibition of acoustic startle in the mouse

status: Public on Mar 30 2017

city: Toronto

first: James

middle: Nicholas

last: Samsom

state: Ontario

address: 544, 155 Dalhousie Street

department: Pharmacology

country: Canada

institute: University of Toronto

summary:
C3H/HeJ, BalbC/J, C57BL/6J, C57BL10/J, C57BLKS/J, C57L/J strains were tested for variability in gene expression in hippocampus, striatal, and brainstem tissues to affiliate findings with behavioural prepulse inhibition scores
Abstract: Current antipsychotic medications used to treat schizophrenia all target the dopamine D2 receptor. Although these drugs have serious side effects and limited efficacy, no novel molecular targets for schizophrenia treatment have been successfully translated into new medications. To identify novel potential treatment targets for schizophrenia, we searched for previously unknown molecular modulators of acoustic pre-pulse inhibition (PPI), a schizophrenia endophenotype, in the mouse. We examined six inbred mouse strains that have a range of PPI, and used microarrays to determine which mRNA levels correlated with PPI across these mouse strains. We examined several brain regions involved in PPI and schizophrenia: hippocampus, striatum and brainstem, and found transcripts that had good correlation with PPI level, and confirmed this with real-time quantitative PCR. We then selected one candidate gene for further study, Pdxdc1 (pyridoxal-dependent decarboxylase domain containing 1), because it is a putative enzyme that could metabolize catecholamine neurotransmitters, and thus might be a feasible target for new medications. We determined that Pdxdc1 mRNA and protein are both strongly expressed in the hippocampus and levels of Pdxdc1 are inversely correlated with PPI across the six mouse strains. Using shRNA packaged in a lentiviral vector, we suppressed Pdxdc1 protein levels in the hippocampus and increased PPI by at least 16%. Our results suggest that Pdxdc1 may regulate PPI and could be investigated further as a potential treatment target for schizophrenia.

overall_design: 18 arrays were sampled per tissue type, 3 arrays per strain of mice, two of which were from control mice (untested for PPI) and one from PPI tested mice, each array had pooled tissue from 3 mice from the experimental group, from alternating hemispheres (e.g. 2 tissue samples from right, 1 from left, and vice versa to balance the whole 3-array set from each strain). 3 tissue types were tested: brainstem, hippocampus, and striatum.

first: Laura

last: Feldcamp

first: Paul

last: Boutros

first: Roger

last: Raymond

first: Jose

middle: N

last: Nobrega

first: Albert

last: Wong


title: Expression data from  PyMT;Lys Cre:E2f3 f/f  TAMs

status: Public on Apr 04 2017

city: Columbus

first: Prashant

last: Trikha

address: 410 W 12 the Av

institute: Ohio State University

summary:
To understand the underlying cause for reduced lung metastasis, we compared global gene expression profiles of F4/80+ FACS sorted tumor-associated macrophages (TAMs)  PyMT;E2f3 f/f (control) and PyMT;Lys Cre:E2f3 f/f (experimental) mice.
We compared gene expression profile between TAMs isolated from mammary tumors of  PyMT;E2f3 f/f and PyMT;Lys Cre:E2f3 f/f mice

overall_design: RNA was extracted from F4/80+ TAMs from mammary tumors of 80 day old mice


title: miR-NC or miR-331-3p treatment of LNCaP prostate cancer cells

status: Public on Mar 23 2017

city: Nedlands

first: Peter

last: Leedman

address: 6 Verdun Street

country: Australia

institute: Harry Perkins Institute of Medical Research

summary: LNCaP prostate cancer cells were treated for 24 hours with either a miRNA negative control (miR-NC) or miRNA 331-3p (miR-331-3p)

overall_design: There were 6 samples in total. 3 x miRNA negative control and 3 x miR-331-3p treated cells. Cells were treated for 24 hours and RNA was harvested at this time point.

first: Michael

middle: R

last: Epis


title: Hepatic transcriptome profiles of mice with diet-induced nonalcoholic steatohepatitis treated with astaxanthin and vitamin E

status: Public on Mar 21 2017

city: Tsukuba

first: Masuko

last: Kobori

state: Ibaraki

address: 2-1-13 Kannondai

institute: Food Research Institute, National Agriculture and Food Research Organization

summary:
Astaxanthin alleviates hepatic lipid accumulation and peroxidation, inflammation, and fibrosis in mice with high-cholesterol, high-cholate, and high-fat (CL) diet-induced nonalcoholic steatohepatitis (NASH). It has been proposed as a potential new treatment to inhibit the progression of NASH in humans. Therefore, we compared hepatic gene expression profiles after treatment with astaxanthin or the antioxidant vitamin E in mice with CL diet-induced NASH. Comprehensive gene expression analyses of the livers of mice fed a standard, CL, or CL diet containing astaxanthin or vitamin E for 12 weeks were performed using a DNA microarray. Both astaxanthin and vitamin E effectively improved gene expression associated with eukaryotic initiation factor-2 (EIF2) signaling, which is suppressed in NASH by endoplasmic reticulum (ER) stress in the liver.
Astaxanthin but not vitamin E was predicted to suppress the actions of ligand-dependent nuclear receptors peroxisome proliferator-activated receptors (PPAR) α and PPARδ and to affect related molecules. Establishing a new therapy using astaxanthin will require elucidation of astaxanthin’s molecular action on the functions of PPARα and related molecules in the livers of mice with diet-induced NASH.

overall_design: 7-week-old C57BL/6J male mice were fed  normal chow (CRF-1) or CL diet (60% calories from fat, 1.25% cholesterol, and 0.5% sodium cholate), CL diet containing 0.02% astaxanthin, or CL diet containing 0.02% vitamin E for 12 weeks.

first: M


title: An epigenomic role of Fe65 in the cellular response to DNA damage.

city: La Jolla

first: MICHAEL

middle: G

last: ROSENFELD

state: CA

address: 9500 Gilman Drive

institute: HHMI/UCSD

type: Genome binding/occupancy profiling by high throughput sequencing

summary: In this study, we hypothesized that the transcriptional activity of Fe65 may contribute to DNA damage pathways by regulating gene expression patterns activated in response to genotoxic stress. To address this hypothesis, we mapped the global binding profile of Fe65 by chromatin immunoprecipitation (ChIP)-sequencing in the SK-N-SH cells exposed to genotoxic stress. Unexpectedly, the genome-wide location analysis showed a substantial enrichment of Fe65 in the promoter regions of coding genes linked to DNA damage signaling pathways.

overall_design:
Fe65 target genes were identified based on the ChIP-seq peaks enriched by Fe65 antibody in SK-N-SH treated with etoposide and compared with non-treated conditions.
------------------------------------
Submitter states "We have submitted the ELAND files as   these were generated very early in 2008, when the first GAIIX Illumina   machines were on the market, and at that time, the machines only did output eland files (the fastq format was introduced at a later time point)."

last: Rosenfeld

first: Francesca

last: Telese

first: Yousin

last: Suh


title: Genome-wide profiling of genes during differentiation of wild (WT) murine embryonic stem cells (ESCs), scrambled control (SCR) ESCs, and Strip2 silenced (KD) ESCs

status: Public on Mar 26 2017

city: Cologne

first: Agapios

last: Sachinidis

state: NRW

address: Robert-Kochstr. 39

department: Institute of Neurophysiology

country: Germany

institute: University of Cologne

summary: The role of Striatin Interacting Protein 2 (Strip2) in differentiation of embryonic stem cells (ESCs) is still under debate. Strip2 silenced (KD) ESCs were differentiated for 4, 8, 12, and 16 days. We show that Strip2 is distributed in the perinucleus or nuclei of wild type (WT) undifferentiated ESCs, but is localized in high-density nuclear bodies in differentiated cells. CellNet analysis of microarray gene expression data for KD and scrambled control (SCR) embryoid bodies (EBs), as well as immunostainings of key pluripotent factors, demonstrated that KD ESCs remain undifferentiated. This occurs even in 16-day old EBs, which possessed a high tumorigenic potential. Correlated with very high expression levels of epigenetic regulator genes, Hat1 and Dnmt3, enzymatic activities of the histone acetyltransferase type B (HAT1) and DNA (cytosine-5)-methyltransferase 3 beta (DNMT3b) were higher in differentiated 16-day old KD EBs than in SCR or WT EBs. The expression levels of let-7, 290 and 302 microRNA families were opposed in KD ESCs, while KD EBs had levels comparable to WT and SCR ESCs during differentiation. This demonstrates that Strip2 is critical to the onset of differentiation, regulating expression of epigenetic regulators, HAT1 and DNMT3b, as well as microRNAs involved in pluripotency.

overall_design: RNA from undifferentiated WT ESCs, SCR ESCS and KD ESCs as well as of 4-, 8-, 12- and 16-day EBs  was  isolated and gene expression was analysed by the Affymetrix (Mouse 430 2.0)  chip


title: Cholera toxin mediates cAMP-dependent CTLA-2 secretion by dendritic cells to induce regulatory T cells in the EAE model

status: Public on Mar 15 2017

city: Wuerzburg

first: Susanne

middle: Elma

last: Kneitz

address: Biozentrum, Am Hubland

department: Physiologigcal Chemistry

institute: University of Wuerzburg

summary: Therapy of autoimmune diseases by tolerogenic dendritic cells (DCs) represents an interesting option for clinical application. Mostly, immature or semi-mature stages of DCs have been shown to convert naïve T cells into FoxP3+ induced regulatory T cells (iTreg). Here we found that murine bone marrow-derived DCs (BM-DCs) matured with cholera toxin (CT) produced cytotoxic T lymphocyte antigen 2 (CTLA-2) via cAMP signaling. CTLA-2 is a cathepsin L inhibitor, however, it exerted cathepsin L-independent tolerogenic functions as shown with cathepsin L knock-out BM-DCs. High or low dose CT (CThi, CTlo) or cAMP treatment of BM-DCs, but not other stimuli such as LPS or TNF, induced mRNA of both isoforms of CTLA-2α and CTLA-2β. CThi-, CTlo- or cAMP-DCs display a mature phenotype (MHC IIhi, costimulationhi). Importantly, only CThi DCs secreted IL-1β, IL-6 and IL-23. Consequently, CThi DCs instructed Th17 cell polarization while, CTlo- or cAMP-DCs induced TGF-β-dependent FoxP3+ iTreg conversion but little or no Th17 cells. iTreg conversion could be reduced by blocking of CTLA-2 with siRNAs and in accordance, addition of recombinant CTLA-2α increased the conversion towards iTreg in vitro. Injection of CTlo- or cAMP-DCs exerted MOG peptide-specific protective effects in experimental autoimmune encephalomyelitis (EAE). Together, we identified CTlo- or cAMP-induced CTLA-2 production by BM-DCs as a tool to enhance their iTreg induction in vitro and in vivo. These findings point to CTLA-2 as a novel mediator of immune evasion by cholera bacteria and its potential use to treat autoimmune diseases.

overall_design: total samples analysed are 6

first: Cinthia

last: Silva Vilches

first: Katrien

last: Pletinckx

first: Miriam

last: Lohnert

first: Vladimir

last: Pavlovic

first: Jie

last: Zhou

first: Rena

last: Chen

first: Thomas

last: Reinheckel

middle: D

last: Mueller

first: Jochen

last: Bodem

first: Manfred

last: Lutz


title: Effect of E-cadherin by N-cadherin replacement in mouse intestinal epithelial cells

city: Freiburg

first: Marc

middle: P.

last: Stemmler

address: Stuebeweg 51

department: Molecular Embryology

institute: Max-Planck Institute of Immunobiology and Epigenetics

summary:
We conditionally substituted E-cadherin (E-cad; cadherin 1) with N-cadherin (N-cad; cadherin 2) during intestine development by generating mice in which an Ncad cDNA was knocked into the Ecad locus
We used microarray to follow gene expression changes derived from lack of E-cadherin on intestinal epithelial cells

overall_design: Epithelial cells were harvested from the small intestine of 14 days old mice harboring N-cadherin and no E-cadherin and from E-cadherin-positive littermates.

first: Rolf

last: Kemler

middle: P

first: Lenka

last: Libusova


title: Comparison of Wild type and Pofut1-deleted skeletal muscle

status: Public on Mar 27 2017

first: Paul

middle: T

last: Martin

state: OH

address: 700 Childrens Dr.

department: Center for Gene Therapy

institute: Nationwide Childrens Hospital

summary:
Pofut1 is an essential gene that glycosylates proteins containing EGF-like repeats, including Notch Receptors (NotchRs).  Work in mice and in Drosophila has shown that O-fucosylation by Pofut1 is required for NotchR ligands to bind to and activate NotchRs.  As such, Pofut1 deletion in skeletal myofibers allows for an analysis of potential functions and molecular changes of Pofut1 in skeletal muscle that derive from its expression in skeletal myofibers. In this study we compared gene expression profiles between quadriceps muscles in mice where Protein O-fucosyltransferase 1 (Pofut1) was deleted specifically in skeletal myofibers via use of a human skeletal alpha actin Cre transgene (Scre) and a loxP flanked Pofut1 gene (SCreFF) and mice which bore the only the Scre transgene but did not have floxed Pofut1 alleles (SCre++).
Muscles were dissected from two month-old mice. We have found that SCreFF mice develop reduced muscle size and strength with age.  These changes are analogous to sarcopenic changes that normally occur in aged muscles, where Pofut1 expression is also reduced.  These phenotypes begin at and beyond 3 months and are very significant by 6 months of age.   The goal of this study was to capture molecular changes that precede the reductions in muscle size and strength, some of which were validated by qRT-PCR.

overall_design: A total of six samples in two groups were analyzed for this study. The first group is three replicates of skeletal α actin cre/Pofut1flox/flox quadriceps. The second group is three replicates of Skeletal α actin cre/Pofut1 wild type quadriceps.

first: Mi-Lyang

last: Kim


title: Microglia-specific microarray analysis at early symptomatic age in a mouse model of amyotrophic lateral sclerosis

status: Public on Mar 10 2017

city: Geneva

first: Celine

last: Delucinge

address: 1 rue Michel Servet

department: iGE3 Genomics Platform

country: Switzerland

institute: University of Geneva

summary: Microarray analysis of microglia in a mouse model of amyotrophic lateral sclerosis identified the dysregulation of Brca1.

overall_design: Microglia were purified by FACS in SOD1 G93A mice and control littermates at P90 days of age. Gene profiles were then compared.

first: Harun

last: Noristani

first: Florence

last: Perrin


title: Expression data from control and Mycobacterium leprae-infected mouse Schwann cells

status: Public on Mar 07 2017

city: Edinburgh

first: Aidan

middle: James

last: McGlinchey

address: 5 Little France Drive

department: Scottish Centre for Regenerative Medicine

country: United Kingdom

institute: University of Edinburgh

summary:
Mycobacterium leprae infect mouse Schwann cells in vitro, reprogram the Schwann cells, and induce mesenchymal stem cell-like cells. In this reprogramming, a vast number of stem cell-related genes, especially those with transcription factor activities are differentially regulated
We used microarrays to detail the global program of gene expression underlying the Mycobacterial infection and identified distinct classes of differentially-regulated genes during this process.

overall_design: Control and Mycobacterium leprae-infected Schwann cells were selected at successive stages of the infection for RNA extraction and hybridization on Affymetrix microarrays. As for infected Schwann cells, three time points including day 14 and day 28 after infection, and the final stage of the reprogramming; pSLC cultured in stem cell media.

first: Toshihiro

last: Masaki

first: Anura

last: Rambukkana


title: Differential expression analysis between Microadenoma and Macroadenoma in Cushing's Disease

city: São Paulo

first: Leonardo

middle: José Tadeu

last: Araújo

address: Av. Dr. Enéas de Carvalho Aguiar, 155, 2 andar, Bloco 6

country: Brazil

institute: HCFMUSP

summary: ACTH-dependent hypercortisolism caused by a pituitary adenoma [Cushing’s disease (CD)] is the most common cause of endogenous Cushing’s syndrome. CD is often associated with several morbidities, including hypertension, diabetes, osteoporosis/bone fractures, secondary infections, and increased cardiovascular mortality. While the majority (≈80%) of the corticotrophinomas visible on pituitary magnetic resonance imaging are microadenomas (MICs, <10 mm of diameter), some tumors are macroadenomas (MACs, ≥10 mm) with increased growth potential and invasiveness, exceptionally exhibiting malignant demeanor. In addition, larger and invasive MACs are associated with a significant increased risk of local complications, such as hypopituitarism and visual defects. Given the clinical and molecular heterogeneity of corticotrophinomas, the aim of this study was to investigate the pattern of genetic differential expression between MIC and MAC, including the invasiveness grade as a criterion for categorizing these tumors. In this study, were included tumor samples from patients with clinical, laboratorial, radiological, and histopathological diagnosis of hypercortisolism due to an ACTH-producing pituitary adenoma. Differential gene expression was studied using an Affymetrix microarray platform in 12 corticotrophinomas, classified as non-invasive MIC (n = 4) and MAC (n = 5), and invasive MAC (n = 3), according to modified Hardy criteria. Somatic mutations in USP8 were also investigated, but none of the patients exhibited USP8 variants. Differential expression analysis demonstrated that non-invasive MIC and MAC have a similar genetic signature, while invasive MACs exhibited a differential expression profile. Among the genes differentially expressed, we highlighted CCND2, ZNF676, DAPK1, and TIMP2, and their differential expression was validated through quantitative real-time PCR in another cohort of 15 non-invasive and 3 invasive cortocotrophinomas. We also identified potential biological pathways associated with growth and invasiveness, TGF-β and G protein signaling pathways, DNA damage response pathway, and pathways associated with focal adhesion. Our study revealed a differential pattern of genetic signature in a subgroup of MAC, supporting a genetic influence on corticotrophinomas in patients with CD.

overall_design: We analyzed RNA from frozen corticotrophinoma from 12 female subjects with Cushing's Disease using the Affymetrix Human Exon 1.0 ST platform (annotation file: HuEx-1_0-st-v2.na33.1.hg19.transcript.csv). Array data was processed by Affymetrix Expression Console 1.3. No technical replicates were performed.

middle: J

first: Ericka

last: Trarbach

first: Antônio

last: Lerario

first: Marcio

last: Machado

first: Marcello

last: Bronstein

first: Maria

last: Fragoso


title: Dido as a switchboard that regulates self-renewal and differentiation in embryonic stem cells (Affy)

status: Public on Mar 16 2017

city: Madrid

first: Carlos

last: Martinez

state: Madrid

address: C/Darwin 3

department: Inmunology and Oncology

country: Spain

institute: Centro Nacional de Biotecnologia

summary:
Transition from symmetric to asymmetric cell division requires precise coordination of differential gene expression. Embryonic stem cells (ESC) strongly express Dido3, whose C-terminal truncation impedes ESC differentiation while retaining self-renewal. We show that Dido3 binds to its gene locus via H3K4me3 and RNA pol II and, at differentiation onset, induces expression of its splice variant Dido1, which then leads to Dido3 degradation and downregulation of stemness genes. We propose that Dido isoforms act as a switchboard to regulate genetic programs for ESC transition from pluripotency maintenance to promotion of differentiation.
We used microarrays to determine how the deletion of exon 16 (C-terminal truncation) of the Dido3 affects gene expression that results in the suppression of ESC differentiation.

overall_design: Stem cells from 2 conditions, wild type and truncated C-terminal Dido3 protein mutant, were cultured in pararell and equal conditions. RNA was extracted and processed for hybridization on Affymetrix microarrays (Affymetrix Mouse Genome 430 2.0 Array). Three biological replicates for each condition were processed simultaneously.

first: Agnes

last: Futterer

first: Jesus

last: De-Celis


title: CancerMap project prostate cancer microarray dataset

status: Public on Mar 13 2017

city: Sutton

first: Colin

last: Cooper

address: 15 Cotswold Rd

department: Oncogenetics

institute: Institute of Cancer Research

summary: Microarray expression profiling has currently failed to provide a consistent classification for human prostate cancer. Such classifications are important because they provide a framework for the identification of new biomarkers of clinical behavior and for the development of targeted therapies. We hypothesize that previous studies have been unsuccessful because of their failure to take into account the well documented occurrence of prostate cancer multifocality and genetic heterogeneity. We have invented a novel method for collecting whole RNALater preserved ‘research slices’ from prostatectomy specimens that, for the first time, allows the mapping of multifocality and of genetic heterogeneity in prostate cancer to be integrated with the selection of samples for expression microarray analysis. For each specimen we will construct a map of the regions of cancer and of their ERG gene rearrangement status from whole mount formalin fixed sections immediately juxtaposed to the ‘research slice’. Only foci of cancers containing a homogeneous pattern of ERG gene alteration will be selected for study. A pilot study has already demonstrated the feasibility of this approach, and provides initial evidence that cancers may be stratified into at least two prognostically distinct categories. Novel biomarkers defining distinct prostate cancer categories will be verified and validated in future studies linked to clinical trials.

sample_organism:
Homo sapiens
Mus musculus

overall_design: 236 samples from fresh frozen tissue from the prostatectomies of 154 prostate cancer patients. 185 samples were from malignant tissue and 51 from morphologically benign tissue. 5 samples are from fibroblasts grown on mice.

first: David

last: Neal

first: Daniel

last: Brewer

first: Hayley

last: Whitaker

first: Sandra

last: Edwards

first: Johanna

last: Burge

first: Marie

last: Corcoran

first: Nening

last: Dennis

first: Tim

last: Dudderidge

first: Rosalind

last: Eeles

first: Cyril

last: Fisher

first: Anne

last: George

first: Steven

last: Hazell

first: Charles

last: Jameson

first: Naomi

last: Livini

first: Lucy

last: Matthews

first: Sue

last: Merson

first: Christopher

last: Ogden

first: Sara

last: Stearn

first: Helen

last: Ross-Adams

first: Roslin

last: Russell

first: Alastair

last: Lamb


title: Identification of JMJD1A and JMJD2B Target Genes in Hypoxic Ovarian Cancer Cells

city: Portland

first: Adam

last: Krieg

state: OR

address: 3181 SW Sam Jackson Park Road, L466

department: OB/GYN

institute: Oregon Health & Science University

summary:
The Hypoxia-Inducible Factors induce the expression of the histone demethylases JMJD1A (KDM3A) and JMJD2B (KDM4B), linking the hypoxic tumor microenvironment to epigenetic mechanisms that may foster tumor progression. Using transcript profiling, we have identified genes that are regulated by JMJD1A and JMJD2B in both normoxic and hypoxic conditions in SKOV3ip.1 ovarian cancer cells.
This dataset includes expression data obtained from exposing ovarian cancer cells to hypoxia in combination with siRNA-mediated knockdown of the hypoxia-inducible histone demethylases JMJD1A and JMJD2B. These data were used to both identify functional overlap between each histone demethylase, as well as identify effectors of tumor growth mediated by JMJD2B (KDM4B) in normoxia and hypoxia.

overall_design:
18 samples were analyzed. The log2-transformed normalized signal intensities were used for downstream pairwise comparisons (using Partek Genomic Suite):
SiControl-Normoxia>SiD1A-Normoxia;
SiD1A-Normoxia>SiControl-Normoxia;
SiControl-Normoxia>SiD2B-Normoxia;
SiD2B-Normoxia>SiControl-Normoxia;
SiControl-Hypoxia>SiControl-Normoxia;
SiControl-Normoxia>SiControl-Hypoxia;
SiControl-Hypoxia>SiD1A-Hypoxia;
SiD1A-Hypoxia>SiControl-Hypoxia;
SiControl-Hypoxia>SiD2B-Hypoxia;
SiD2B-Hypoxia>SiControl-Hypoxia.

first: Lei

last: Qiu


title: Genome-wide profiling of genes and miRNAs during differentiation of wild (WT) murine embryonic stem cells (ESCs), scrambled control (SCR) ESCs, and Strip2 silenced (KD) ESCs

first: Agapios

last: Sachinidis

type:
Expression profiling by array
Non-coding RNA profiling by array

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

platform_organism:
Mus musculus
synthetic construct

overall_design: Refer to individual Series


title: Expression data from induced pluripotent stem cells (iPSCs), mouse embryonic stem cells (mESCs), and mouse embryonic fibroblast (MEFs)

status: Public on Mar 09 2017

city: Taipei

first: I-I

last: KUAN

address: 128 Sec.2 ﹐Academia Rd ﹐

department: Institute of Cellular and Organismic Biology

country: Taiwan

institute: Acdamic Sinica

summary:
During reprogramming of mouse embryonic fibroblast, pluripotent genes are up-regulated. Once iPSCs are successfully reprogrammed, the global gene profiles of iPSCs are comparable to mouse ESC.
We used microarrays to detail the global programme of gene expression in iPSCs, mESCs, MEFs.

overall_design: We picked four clones of iPSCs, three clones of mESCs, and one mouse embryonic fibroblast (MEF) primary culture cells for microarrays.

last: Kuan

first: Shang-Chih

last: Yang


title: Evaluation of in vitro macrophage differentiation during space flight

city: Mountain View

first: NASA

last: GeneLab

address: Mail Stop N211

institute: NASA Ames Research Center

summary:
We differentiated mouse bone marrow cells in the presence of recombinant macrophage colony stimulating (rM-CSF) factor for 14 days during the flight of space shuttle Space Transportation System (STS)-126. We tested the hypothesis that the receptor expression for M-CSF, c-Fms was reduced. We used flow cytometry to assess molecules on cells that were preserved during flight to define the differentiation state of the developing bone marrow macrophages; including CD11b, CD31, CD44, Ly6C, Ly6G, F4/80, Mac2, c-Fos as well as c-Fms. In addition, RNA was preserved during the flight and was used to perform a gene microarray. We found that there were significant differences in the number of macrophages that developed in space compared to controls maintained on Earth. We found that there were significant changes in the distribution of cells that expressed CD11b, CD31, F4/80, Mac2, Ly6C and c-Fos. However, there were no changes in c-Fms expression and no consistent pattern of advanced or retarded differentiation during space flight. We also found a pattern of transcript levels that would be consistent with a relatively normal differentiation outcome but increased proliferation by the bone marrow macrophages that were assayed after 14 days of space flight. There also was a surprising pattern of space flight influence on genes of the coagulation pathway. These data confirm that a space flight can have an impact on the in vitro development of macrophages from mouse bone marrow cells.
MESH:Space Flight/Space Flight

overall_design: transcription profiling of 2 total treatment groups and 4 total samples

first: Stephen

middle: K

last: Chapes


title: Il-22-Fc in cutaneous wound healing response

status: Public on Mar 08 2017

city: South San Francisco

first: Mark

last: McCreary

state: California

address: 1 DNA Way, MS 93

department: Bioinformatics

institute: Genentech

summary: Diabetic foot ulcers (DFU) are one of the major complications in type II diabetes patients and can result in amputation and morbidity. Although multiple approaches are used clinically to help wound closure, many patients still lack adequate treatment. Here we show that IL-20 subfamily cytokines are upregulated during normal wound healing. While there is a redundant role for each individual cytokine in this subfamily in wound healing, mice deficient in IL-22R, the common receptor chain for IL-20, IL-22, and IL-24, display a significant delay in wound healing. Furthermore, IL-20, IL-22 and IL-24 are all able to promote wound healing in type II diabetic db/db mice. When compared to other growth factors such as VEGF and PDGF that accelerate wound healing in this model, IL-22 uniquely induced genes involved in reepithelialization, tissue remodeling and innate host defense mechanisms from wounded skin. Interestingly, IL-22 treatment showed superior efficacy compared to PDGF or VEGF in an infectious diabetic wound model. Taken together, our data suggest that IL-20 subfamily cytokines, particularly IL-20, IL-22, and IL-24, might provide therapeutic benefit for patients with DFU.

overall_design: There are 45 samples in total (nine groups n=5/group). We have prepared the RNA from Diabetic Foot Ulcer Skin wounds. The following is the experimental design: Groups 1-4: 24 hrs time point; Groups 5-9: day7 post wound; Group 1: db/db females, n=5, anti Ragweed; Group 2: db/db females, n=5 IL-22 Fc; Group 3: db/db females, n=5 VEGF; Group 4: db/db females, n=5 PDGF; Group 5: dbm females n=5, PBS (lean control mice); Group 6: db/db females, n=5, anti-Ragweed; Group 7: db/db females, n=5 IL-22 Fc; Group 8: db/db females, n=5 VEGF; Group 9: db/db females, n=5 PDGF anti-Ragweed (50 ug) and Il-22 Fc (20 ug). For groups 1-4, wound (6mm) will be created on Day0 and receive one dose of topical treatment. Mice will be euthanized 24 hrs post topical treatment and wound tissue will be harvested. For groups 5 through 9 wound will be created on day 0 and dosed topically on Day0, Day2, day4, day 6. Mice will be euthanized on Day 7 and wound tissue harvested and RNA prepared.

first: Ganesh

last: Kolumam

first: Xiumin

last: Wu

first: Wyne

last: Lee

first: Jason

middle: A

last: Hackney

first: Jose

last: Zavala-Solorio

first: Vineela

last: Gandham

first: Dmitry

last: Danilenko

first: Puneet

last: Arora

first: Wenjun

last: Ouyang

first: Xiaoting

last: Wang


title: Identification of potential ABBV-075 responsive markers in mouse whole blood

city: North Chicago

first: Xin

last: Lu

state: IL

address: 1 North Waukegan Rd

department: Oncology Discovery

institute: Abbvie

summary: To identify genes that are modulated by BET inhibitors in blood, we determined global gene expression changes in ABBV-075-treated mouse whole blood samples

overall_design: Mice were dosed with vehicle, 1 mg/kg or 5 mg/kg ABBV-075 for 6 hours, and whole blood was collected and subjected to total RNA extration and miroarray analysis. Each dosing group contains 5 mice.

first: Tamar

last: Uziel

first: Paul

last: Hessler

first: Daniel

last: Albert


title: Pten deletion in neonatal brain induces an abnormal neural progenitor niche that can synergize with Trp53 loss to generate medulloblastoma

status: Public on Mar 01 2017

city: Memphis

first: David

last: Finkelstein

state: TN

address: 332 N. Lauderdale St.

department: Computational Biology

institute: St Jude Children's Research Hospital

type: Genome variation profiling by genome tiling array

summary: To investigate Pten function in neonatal developing brain, we conditionally inactivated Pten in neural stem/progenitor cells at birth using a Nestin-CreER transgenic driver. Pten inactivation created a novel perivascular proliferative niche in the cerebellum that did not progress to malignancy during the lifespan of the mouse.  Co-deletion of Pten and Trp53 synergized to cause fully penetrant medulloblastoma originating from a perivascular niche. The Pten and Trp53 double knock-out medulloblastomas showed an extensive and abnormal blood vessel network and advanced neuronal differentiation of tumor cells compared to medulloblastomas arising in Nestin-creER;Trp53fl/fl mice, suggesting that Pten loss promoted angiogenesis and neuronal differentiation in medulloblastoma. EdU pulse-chase experiments demonstrated a lineage hierarchy of the double knock-out medulloblastomas consistent with a perivascular cancer stem cell population. The Pten and Trp53 double knock-out medulloblastomas showed somatic loss of chromosomes 7, 13 and 16, and inactivating mutations in the tumor suppressor gene Ptch1. Gene expression profiles showed that this model recapitulated the subgroup of human medulloblastomas with de-regulated SHH signaling.

overall_design:
Copy number changes of this Medulloblastoma model was investigated using aCGH for 18 tumors. Gene expression profiling was done using Affymetrix HG-U133 plus 2 arrays for 6 tumors, 3 mouse brain with Pten wildtype at P5, 3 mouse brain with Pten null at P5, 3 mouse brain at adult age.

The double knockout mouse are mixed background of FVB and C57BL/6.

first: Guo

last: Zhu

first: Suzanne

last: Baker


title: Expression data from brains of BCAS1 knockout or wildtype mice

city: Sapporo

first: Kensuke

last: Ninomiya

address: Kita-15, Nishi-7, Kita-Ku

institute: Hokkaido University

summary: We used microarrays to compare the expression profiles between brains of BCAS1 knockout and wild type mice

overall_design: Brains of BCAS1 knockout or wild type mice were dissected for Total RNA isolation and hybridization on Microarray.

first: Tetsuya

last: Ishimoto


title: Real-time quantitative RT-PCR analysis of mouse antigen specific T cells (CD8+Spas1)

status: Public on Feb 28 2017

city: San Frnacisco

first: Chien-Chun

middle: Steven

last: Pai

address: 513 Parnassus Ave

department: Hematology Oncology

institute: UCSF

summary: In this experiment, we seek to evalulate the apoptotic gene expression on antigen specific T cells. (CD45+CD3+CD8+Spas-1) after different checkpoint inhibitors treatments

overall_design: Mice were implanted with TRAMP-C2 tumors(10^6/mouse) at Day 0 and treated with different checkpoint inhibitors, including anti-CTLA-4, anti-PD-1 DANA, Combo DANA, isotype. Draining lymph nodes were harvested at Day 28. Five mice from each group were pooled together and sorted on CD45+CD3+CD8+Spas-1 antigen specific T cells. Sorted cells were dissolved in RNA later and subsequent for RNA extraction and cDNA generation. RT-PCR array were run on Qiagen kit and analysed on Qiagen website under data analysis center

first: Katsunobu

last: Hagihara


title: Gene expression data from OVA-immunized WT and Rptor-/- follicular regulatory T cells

status: Public on Feb 20 2017

city: Chongqing

first: Lifan

last: Xu

address: 30 Gaotanyan Street

department: Institute of Immunology, PLA

country: China

institute: Third Military Medical University

summary:
Follicular regulatory T (Tfr) cells maintain homeostasis of humoral immunity by suppressing germinal center responses. TFR cells are differentiated from conventional regulatory T (Treg) cells, but underlying mechanisms remain largely unknown.
We did microarray experiments to elucidate the transcriptome changes due to Rptor deficiency in Tfr cells. These data clearly demonstrate that Tfr-associated genes were down-regulated in Rptor-null Tfr cells, indicating that Raptor regulate Tfr generation by strengthening Tfr signatures.

overall_design: We first sorted WT (1 sample, pooled from 4 mice) and Rptor-null Tfr cells (2 samples, each sample pooled from 8 mice) at day 8 after OVA immunization. Then, we extracted RNA, which were subsequently sent to microarray analysis.

first: Lilin

last: Ye

first: Yuzhang

last: Wu


title: Transcriptome_Methylome_Sirt1KOESC

city: Seoul

first: DONG-MYUNG

last: SHIN

address: Pungnap-2 dong, Songpa-gu

department: Department of Biomedical Sciences

country: South Korea

institute: University of Ulsan College of Medicine

type: Methylation profiling by genome tiling array


status: Public on Feb 15 2017

city: Tianjin

first: Shan

last: Gao

address: No 94, weijin road

institute: Nankai University

summary: Comparing to matched normal mucosa, WTX was lost in most of human colorectal cancers (Zhang et al., 2016). We analyzed the microRNA expression profiling among WTX low human colorectal cancer tissues and matched adjacent WTX high normal colorectal mucosa. The aimed to identify the unique signature of miRNAs which related to WTX loss in human colorectal cancers.

platform_organism:
Homo sapiens
Mus musculus
Rattus norvegicus
Human gammaherpesvirus 8
Macacine gammaherpesvirus 4
Betapolyomavirus macacae

overall_design: We performed microRNA expression profiling on 5 patients who were WTX low in colorectal cancers and WTX high in matched normal mucosa samples.

first: Qingling

last: Zhang

first: Guifang

first: Huilin

last: Niu

first: Qiming


title: MMS induced expression changes (Mouse)

status: Public on Feb 14 2017

city: San Antonio

first: Yidong

last: Chen

state: Texas

address: 8403 Floyd Curl Drive, MSC 7784

department: Population Health Sciences

institute: UT Health Science Center at San Antonio

summary: Despite the high toxicity, alkylating agents are still at the forefront of several clinical protocols used to treat cancers. In this study, we investigated the mechanisms underlying alkylation damage responses, aiming to identify novel strategies to augment alkylating therapy efficacy. In this pursuit, we compared gene expression profiles of evolutionary distant cell types (D. melanogaster Kc167 cells, mouse embryonic fibroblasts and human cancer cells) in response to the alkylating agent methyl-methanesulfonate (MMS). We found that many responses to alkylation damage are conserved across species independent on their tumor/normal phenotypes. Key amongst these observations was the protective role of NRF2-induced GSH production primarily regulating GSH pools essential for MMS detoxification but also controlling activation of unfolded protein response (UPR) needed for mounting survival responses across species. An interesting finding emerged from a non-conserved mammalian-specific induction of mitogen activated protein kinase (MAPK)-dependent inflammatory responses following alkylation, which was not directly related to cell survival but stimulated the production of a pro-inflammatory, invasive and angiogenic secretome in cancer cells. Appropriate blocking of this inflammatory component blocked the invasive phenotype and angiogenesis in vitro and facilitated a controlled tumor killing by alkylation in vivo through inhibition of alkylation-induced angiogenic response, and induction of tumor healing.

overall_design: Gene expression of four biological replicates of primary C57BL6/J mouse embryonic fibroblasts. Cell were plated and medium was exchanged 24 hours later for media either without (Ctrl) or with MMS (MMS at 40 µg/mL) treatment. RNA was harvested either 0, 1, 8, 24 or 72 hours following initiation of MMS exposure.

first: Alfeu

last: Zanotto-Filho

first: Ravi

last: Dashnamoorthy

first: Pragathi

last: Masamsetti

first: Eva

last: Loranc

first: Subapriya

last: Rajamanickam

first: Ana

middle: V

last: Chavez-Santoscoy

first: Sonal

last: Tonapi

first: Robert

middle: L

last: Reddick

first: Uthra

last: Suresh

first: Alexander

last: Bishop


title: MMS induced expression changes

sample_organism:
Drosophila melanogaster
Mus musculus

platform_organism:
Drosophila melanogaster
Mus musculus


title: Skn-1-deficient effect on the gastrocnemius

status: Public on Feb 11 2017

city: Bunkyo-ku

first: Shota

last: Ushiama

address: 1-1-1 Yayoi

institute: The University of Tokyo

summary:
Analysis of gastrocnemius from male wild type(WT) and Skn-1-deficient mice. Skn-1-deficient mice have reduced body weight with low body fat due to increased energy expenditure.
Results provide insight into the molecular mechanisms up-regulating metabolism.

overall_design: Using Affymetrix Mouse Genome 430 2.0 Array, we compared global gene expression on the gastrocnemius between Skn-1-deficient mice and WT mice after 18h fasting

first: Keiko

last: Abe


title: Expression data from 3 different Reeler mouse models

city: Boston

first: Uwe

last: Beffert

address: 24 Cummington Mall

department: Biology

institute: Boston University

summary:
The goal of the study was to determine global expression differences and commanlities in three different Reeler mutant mosue models. Phenotypically mice deficient in Reelin, Dab1 or both Reelin receptors apoEr2 and Vldlr exhibit a severe Reeler phenotype.
We used microarrays to detail the global programme of gene expression changes occurring in the frontal cortex of three different mouse models which each generate a Reeler phenotype.

overall_design: Offspring from Reeler +/- matings, Dab1 +/- matings and double heterozygote apoER2 / Vldlr mice were bred and offspring were collected at 21 days after birth.

first: Beffert

last: Uwe

first: Ho

last: Angela


title: Therapeutic vulnerabilities of mesenchymal subpopulations of pancreatic cancer cells undergoing anabolic reprogramming [set2]

status: Public on Feb 13 2017

city: Houston

first: Giannicola

last: Genovese

state: TX

address: 1901 East Road

department: Genomic Medicine

institute: UTMDACC

summary: Malignant neoplasms adapt and evolve in response to changes in oncogenic signaling, tumor microenvironmental stresses,and therapeutic interventions. Cancer cell plasticity in response to these evolutionary pressures is foundational to tumor progression and maintenance and therapeutic resistance. Here, to elucidate the underlying molecular and cellularmechanisms of cancer cell plasticity, integrated system-level, functional and genetic analyses were conducted in a conditional oncogenic Kras model of pancreatic ductal adenocarcinoma (PDAC), amalignancy displaying remarkable phenotypic diversityand morphological heterogeneity. In this model, stochastic extinction of oncogenic Krassignaling and emergence ofKras-independent escaper populationsis associated withde-differentiation and aggressive biological behavior.Transcriptomic and functional analyses ofKras-independent escapers reveal mesenchymal reprogramming driven by aSmarcb1/Mycnetwork and independence from MAPK signaling.A somatic mosaic model of PDAC which can track evolving subpopulations shows that depletion of Smarcb1 activates theMyc network which results in an anabolic switch to increased protein metabolism and the adaptive activation of ERstress-induced survival pathways.Theelevated protein turnover made mesenchymal sub-populationshighly susceptible topharmacological and genetic perturbation of the cellular proteostatic machinery andthe IRE1-α/MKK4 arm of the ER stress response pathway. Specifically, combination regimens impairing the unfolded protein responses (UPR) and the ER stress response can block the emergence of aggressive mesenchymal subpopulations in murine andpatient-derived PDACmodels. These molecular and biological insights inform a potential therapeutic strategy fortargeting aggressive mesenchymal features of PDAC.

overall_design: Smarcb1 deficient pancreatic tumors were treated with tamoxifen to induce restoration to the physiological level of Smarcb1 expression. Vehicle treated tumors were used as controls. Five indepedent biological replicates per each of two groups were processed on Affymetrix Mouse 430_2 microarray platform. Resulting CEL files were imported into Gene Pattern software from the Broad Institute, and converted to normalized GCT format using default parameters in module, ExpressionFileCreator. Normalized GCT table format was used for Gene Set Enrichment Analysis (GSEA) using GSEA software provided by the Broad Institute, Cambridge MA.

first: Genovese

last: Giannicola


title: Therapeutic vulnerabilities of mesenchymal subpopulations of pancreatic cancer cells undergoing anabolic reprogramming [set 1]

overall_design: Kras mutant pancreatic epithelial cells were cultured under oncogenic stress. Spontaeneous senescence escapers were isolated, expanded and functionally characterized. Four indepedent biological replicates per each of two groups were processed on Affymetrix Mouse 430_2 microarray platform. Resulting CEL files were imported into Gene Pattern software from the Broad Institute, and converted to normalized GCT format using default parameters in module, ExpressionFileCreator. Normalized GCT table format was used for Gene Set Enrichment Analysis (GSEA) using GSEA software provided by the Broad Institute, Cambridge MA.


title: Gene expression in human lymphoblastoid cell-line GM12878 in response to sulforaphane treatment

status: Public on Feb 18 2017

city: Research Triangle Park

first: Xuting

last: Wang

address: 111 TW Alexander Dr

institute: NIEHS/NIH

summary:
To determine if induced NRF2 binding is associated with gene expression in genome-wide. We examined mRNA levels with theAffymetrix Human Exon 1.0 ST platform in human lymphoblastoid GM12878 cells treated with sulforaphane to activate NRF2.
Nrf2, a basic leucine zipper transcription factor encoded by the gene NFE2L2, is a master regulator of the transcriptional response to oxidative stress. Nrf2 is structurally and functionally conserved from insects to humans, and it heterodimerizes with the small Maf transcription factors to bind a consensus DNA sequence (the antioxidant response element, or ARE) and regulate gene expression. In this study, we use chromatin immunoprecipitation (ChIP-seq) and gene expression data to identify direct Nrf2 target genes in human and Drosophila.

overall_design: Human lymphoblastoid (GM 12878) cells at a density of 900,000 cells/ml were prepared in triplicate for each time point and treated with 10 µM D,L-sulforaphane (Calbiochem) for  8, 24 hr or no treatment (at 0 time). Total RNA will be extracted from each culture (9 RNA samples) using the Qiagen RNeasy kit with DNase digestion. RNA was quantified using RiboGreen (Invitrogen), check for quality by OD and Bioanalyzer and stored at -80°C.  Expression analysis was conducted at at NIEHS Microarray Core using Affymetrix Human Exon 1.0 ST arrays following the Affymetrix hybridization protocols. Exon expression data were analyzed through Affymetrix Expression Console using gene-level RMA summarization and sketch-quantile normalization methods.

first: Michelle

last: Campbell

first: Douglas

last: Bell


title: Therapeutic vulnerabilities of mesenchymal subpopulations of pancreatic cancer cells undergoing anabolic reprogramming


title: Genomewide gene expression analysis of murine Sirt1 wild-type or knock-out embryonic stem cells (ESCs)

first: DONG-MYUNG

last: SHIN

summary:
Stem-cells and transformed cancer cells specifically express a polycomb repressive complex subtype, PRC4 which characteristically contains Sirt1 (Sirtuin-1), a NAD+ dependent class III histone deacetylase (HDAC) and Eed2 isoform as specific members.  Analyzing the transcriptiome and methylome analysis of Sirt1 deficient murine ESCs (Sirt1-/- ESC), we demonstrate that these cells repressed specifically on some genomic imprinted and germ-line related genes.
We used microarrays to characterize the programm of gene expression affected by Sirt1 in murine ESCs and identified distinct classes of down-regulated genes upon Sirt1 deficiency

overall_design: Total RNA were prepared from the Sirt1 wild-type and mutant ESCs and hybridization on Affymetrix microarrays were performed. The Wild-type and Sirt1 deficient murine R1 ESCs were grown in ESC medium supplemented with 100 IU/ml ESGRO/LIF under 0.1% gelatin coated tissue culture dish.

first: Dong-Myung

last: Shin

first: Mariusz

last: Ratajczak


title: Identification of potential ABBV-075 responsive markers in mouse skin

first: Xin

last: Lu

summary: Determination of transcriptional alterations in skin samples from ABBV-075 treated mice

overall_design: Mice were dosed with vehicle, or 1 mg/kg  ABBV-075,  skin was collected 6 hours and 24 hours post dosing and subjected to total RNA extraction and miroarray analysis.  Vehicle group contains 3 mice and ABBV-075 dosing group contains 4 mice

first: Tamar

last: Uziel

first: Paul

last: Hessler

first: Daniel

last: Albert


title: Whole-transcriptome expression data from neonatal rat ventricular myocytes (NRVM) silenced for KChIP2

city: Columbus

first: Thomas

last: Hund

address: 473 W 12th Ave

institute: Ohio State University

summary: Loss of KChIP2 during cardiac stress has been suggested to have a transcriptional impact on cardiac ion channels  contributing to maladaptive electrical remodeling. Therefore, we tested the consequence of KChIP2 loss, in the absence of cardiac stress, by treating cultured neonatal rat ventricular myocytes with shRNA for KChIP2 and subsequently performed whole-transcriptome microarray analysis to identify gene changes.

overall_design: NRVMs were isolated from the hearts of neonatal (day 1-2) Sprague Dawley rats. They were subsequently plated and cultured for 24-36 hrs then treated with either a control or KChIP2 shRNA inserted into a adenoviral construct. Cells were left in culture for an additional 48 hrs following shRNA delivery, after which they were collected for total RNA.


title: Distinct skeletal muscle gene regulation from active contraction, passive vibration, and whole body heat stress in humans

status: Public on Feb 09 2017

city: Iowa City

first: Richard

last: Shields

address: 1-252 Medical Education Building

institute: The University of Iowa

summary: We used a novel approach to study the acute effect of three physiologic stressors (active contractions, vibration, and systemic heat stress) in human skeletal muscle. Three hours after the completion of a dose of physiologic stress, we sampled the soleus (contraction and vibration) or vastus lateralis (heat) muscle and developed a unique gene expression signature for each stressor. We discovered repetitive active muscle contractions up regulated metabolic transcription factors NR4A3 (12.45 fold change), PGC-1α (5.46 fold change), and ABRA (5.98 fold change); and repressed MSTN (0.56 fold change).  Heat stress repressed PGC-1α (0.74 fold change); while vibration induced FOXK2 (2.36 fold change).  Vibration similarly caused a down regulation of MSTN (0.74 fold change), but to a lesser extent than active muscle contraction.  Vibration induced FOXK2 while heat stress repressed PGC-1α (0.74 fold change) and ANKRD1 genes (0.51 fold change).  These findings support a distinct gene regulation in response to heat stress, vibration, and muscle contractions.  Understanding these responses may assist in developing regenerative rehabilitation interventions to improve muscle cell development, growth, and repair.

overall_design: We analyzed skeletal muscle using the Affymetrix Human Exon 1.0 ST platform. Array data was processed by Partek Genomic Suites.

first: Michael

last: Petrie

first: Colleen

last: McHenry

first: Amy

last: Kimball

first: Chu-Ling

last: Yen

first: Arpit

last: Sharma

first: Manish

last: Suneja


title: Gene expression profiles in the colon of APC and Olfm4 double mutant mice

city: Bethesda

first: WeiPing

last: Chen

state: MD

address: Bldg 8, Room 1A11, NIDDK/NIH

department: GCL

institute: NIDDK/NIH

summary: APC mutant mice develop polys in the intestine, but not carcinoma. We found that additional deletion of Olfm4 gene induced carcinoma formation in the distal colon. To explore the molecular mechanism, we performed cDNA microarray to understand the gene expression files in the tumor tissues compared with WT, APC mutant and Olfm4 mutant mice.

overall_design: RNA were extracted from three mice of each genotyp category, WT, APC mutant, Olfm4 mutant, APC/Olfm4 mutant adjacent tissues and APC/Olfm4 tumor tissues. Affymetrix Mouse Genome 430 2.0 Array GeneChips were used to invesstigate gene expression patterns. The expression files in different groups were compared.

first: Griffin

last: Rodgers

first: Wenli

last: Liu

first: Hongzhen

last: Li

first: Weiping


title: Axonal Lesion-Induced Dpysl3 mRNA Expression in Immature Neurons is Unaffected by Myelin-Specific T Cells

status: Public on Feb 01 2017

city: odense

first: mads

last: thomassen

address: soender boulevard 29

country: Denmark

institute: odense university hospital

summary: Knowing the effect of autoimmune CNS-targeting T cells on the expression of neurogenesis-associated genes is essential to understand their putative effect on hippocampal functioning. Here, we used RNA microarray analysis to study the effect of myelin-specific T cells on the gene profile in the dentate gyrus 2 days after a perforant pathway transection, when neural precursor cells are highly proliferating. By the use of Gene Ontology analysis, the MANGO database and the Allan Mouse Brain Atlas, we identified dihydropyrimidinase-like 3 (Dpysl3), due to its expression in the subgranular zone of the dentate gyrus. In situ hybridizations and quantification of Dpysl3 mRNA+ grains in the subgranular zone and granular cell layer showed a significant increase in Dpysl3 mRNA in axonal lesioned compared to control mice, and no effect of the myelin-specific T cells. Dpysl3 mRNA was not expressed in Ki-67 mRNA+ proliferating cells and NeuN mRNA+ mature neurons, but it was expressed in Nestin mRNA+ neural precursor cells and even more so in Dcx mRNA+ migrating neuroblasts. These results suggest that the regulation of Dpysl3 mRNA expression in immature granular neurons is refractory to inflammatory mediators secreted by the myelin-specific T cells, while being highly responsive to neuronal stimuli. Comparable mechanisms may support normal hippocampal functioning in diseases characterized by infiltration of autoimmune CNS-targeting T cells, such as multiple sclerosis.

overall_design: To allow the identification of T cell up- and downregulated transcripts involved in axonal lesion-induced neurogenesis, we compared the gene expression values in hippocampi of AxL (n=5) to TPlp+AxL (n=5) mice by the use of RNA microarray analysis.

first: Manuela

last: Grebing

first: Mads

last: Thomassen


title: Gene expression profiles of KDM5A-/- MEFs with wild-type KDM5A or KDM5A-H483A mutant

status: Public on Feb 08 2017

city: New Haven

first: Qin

last: Yan

state: CT

address: 310 Cedar St

department: Pathology

institute: Yale University

summary: Gene expression profiles of Immortalized KDM5A-/- MEFs with re-introduction of wild-type KDM5A or KDM5A-H483A mutant.

overall_design: Duplicate total RNA samples were isolated from subconfluent MEFs using RNeasy mini kit with on-column DNase digestion (Qiagen). Gene-expression profiling was performed using Affymetrix mouse M430 2.0 chip.

first: Zongzhi

first: William

last: Kaelin Jr


title: PACAP induces adult neural progenitor surface attachment by increasing the production of extracellular matrix components

city: Warsaw

first: Pawel

last: Niewiadomski

address: Banacha 2c

department: Centre of New Technologies

country: Poland

institute: University of Warsaw

summary: New neurons are born throughout the life of mammals in germinal zones of the brain known as neurogenic niches: the subventricular zone of the lateral ventricles and the subgranular zone of the dentate gyrus of the hippocampus. These niches contain a subpopulation of cells known as adult neural progenitors (aNPCs), which self-renew and give rise to new neurons and glia. aNPCs are regulated by many factors present in the niche, including the extracellular matrix (ECM). We show that the neuropeptide PACAP (pituitary adenylate cyclase-activating polypeptide) affects subventricular zone-derived aNPCs by increasing their surface adhesion. Gene array and reconstitution assays indicate that this effect can be attributed to the regulation of ECM components and ECM-modifying enzymes in aNPCs by PACAP. Our work suggests that PACAP regulates a bidirectional interaction between the aNPCs and their niche:  PACAP modifies ECM production and remodeling, in turn the ECM regulates progenitor cell adherence.  We speculate that PACAP may in this manner help restrict adult neural progenitors to the stem cell niche in vivo, with potential significance for aNPC function in physiological and pathological states.

overall_design: aNPCs were treated for 24, 48, or 96 hours with either vehicle or 10nM PACAP (6 conditions total). RNA was collected and pooled from 5-6 experiments per group and the resulting RNA was processed and hybridized to one Affymetrix Mouse 430 v2 per treatment condition (6 arrays total - 3 control samples and 3 PACAP-treated samples).

first: Joseph

last: Cohen

first: James

last: Waschek


title: Advax, a delta inulin microparticle, potentiates in-built adjuvant property of co-administered vaccines

status: Public on Jan 31 2017

city: Ibaraki

first: Yoshinobu

last: Igarashi

state: Osaka

address: 7-6-8 Asagi-Saito

institute: National Institutes of Biomedical Innovation, Health and Nutrition

summary:
Gene expression data from mouse organs after Advax injection
Advax, an inulin-derived microparticle, has been developed as an adjuvant for several vaccines. Advax is a unique class of adjuvant which can potentiate the endogenous adjuvant effect of the vaccines through a not yet fully-identified, unique mechanisms of action.

overall_design: C57BL/6J mice (6 week old, male, n = 2 or 3) were injected i.d. or i.p. with a total volume of 1000ug of Advax in PBS. The vehicle-control mice (n = 2 or 3) were injected with the same volume of PBS. After 6 h, the inguinal LNs, liver, kidney and spleen were removed (within one hour for all samples) and grobal gene expression was obtained by Affymetrix GeneChip.

first: Masayuki

last: Hayashi

first: Taiki

last: Aoshi

first: Yasunari

last: Haseda

first: Kouji

last: Kobiyama

first: Edward

last: Wijaya

first: Noriyuki

last: Nakatsu

first: Daron

middle: M

last: Standley

first: Hiroshi

last: Yamada

first: Yoshikazu

last: Honda-Okubo

first: Hiromitsu

last: Hara

first: Takashi

last: Saito

first: Toshiyuki

last: Takai

first: Cevayier

last: Coban

first: Nikolai

last: Petrovsky

first: Ken

last: Ishii


title: Expression data from thalamic nuclei in control and bilateral enucleated mice at P0 and P4

status: Public on Jan 30 2017

city: San Juan de Alicante

first: Guillermina

last: López-Bendito

state: Alicante

address: Av. Ramón y Caja,Campus de San Juan

department: Instituto de Neurociencias CSIC

institute: Universidad Miguel Hernández

summary:
Elimination of peripheral retinal axons leads to changes in gene expression in both visual and somatosensory thalamic neurons.
We used microarrays to determine the global programme of gene expression underlying peripheral input deprivation and identify candidate thalamic genes involved in cross-modal plasticity.

overall_design: Mouse thalamic tissue from identified nuclei was selected at two postnatal stages P0 and P4 for RNA extraction and hybridization on Affymetrix microarrays. We used two conditions: controls (non-enucleated) and embryonically bilateral enucleated (embBE) mice. Each sample is composed by pooling the thalamic nuclei tissue from pups from the same litter and same condition.

first: Cecilia

last: Mezzera

first: Verónica

last: Moreno-Juan


title: Pairwise Gene Expression Comparison between Gleason 3 and Gleason 4 Prostate Cancer

first: Adam

middle: G.

last: Sowalsky

address: 37 Convent Drive Building 37 Room 1062B

department: Genitourinary Malignancies Branch

institute: National Cancer Institute

summary:
In this dataset, we report the gene expression of adjacent Gleason 3 and Gleason 4 foci microdissected from the same prostate cancer sample.
We found a striking similarity between adjacent G3 and G4 tumors, consistent with their clonal origin, but very few recurrently up- or down- regulated genes across patients.

overall_design: 26 samples were analyzed in total: 13 pairs of G3 and G4 tumors. Pairwise comparisons are G4 vs. G3. Total RNA was prepared for hybridization using NuGEN Ovation, Exon and Biotinylation kits.

first: Huihui

last: Ye

first: Zheng

last: Xia

first: Wei

last: Li

first: Steven

last: Balk


title: Molecular characterization of the genital organizer: Gene expression profile of the mouse urethral plate epithelium (GUDMAP Series ID: 51)

city: Edinburgh

first: GUDMAP

last: Developers

address: Crewe Road

institute: IGMM MRC Human Genetics Unit

summary: Lower urinary tract malformations are among the most common congenital anomalies in humans. The urethral plate epithelium is an endodermal signaling region that plays an essential role in external genital development; however, little is known about the molecular identity of this cell population or the genes that regulate its activity. We aim to characterize differences in gene expression between the urethral plate epithelium and surrounding mouse genital tubercles during a crucial developmental period.

overall_design: E12.5 transgenic embryos (Shhtm1(EGFP/cre)Cjt / Gt(ROSA)26Sortm3(CAG-EYFP)Hze) were harvested and the genital tubercle dissected from them. Shh expressing urethral epithelial cells were isolated from non-Shh expressing cells of the genital tubercle cells using FACS sorting techniques.

first: Martin

last: Cohn

first: Brooke

last: Armfield


title: The human blood transcriptome following sleep extension and sleep restriction: Heterozygote samples

city: Guildford

first: Emma

last: Laing

address: Stag Hill

institute: University of Surrey

summary: In a cross balanced design human subjects were given one week of sufficient sleep and insufficient sleep (6 h per day). Following each of these conditions they were then kept awake for a day, a night and the subsequent day. During each of these periods of extended wakefulness 10 blood samples were taken, RNA was extracted from leukocytes, labelled and hybridised to human whole-genome microarrays

overall_design: A total of 49 samples comprising 10 human subjects, for which three samples across multiple time-points/sleep conditions were collected.

first: Carla

last: Moller-Levet

first: Simon

last: Archer

first: Giselda

last: Bucca

first: Ana

last: Slak

first: Renata

last: Kabiljo

first: June

last: Lo

first: Nayantara

last: Santhi

first: Malcolm

last: von Schantz

first: Colin

last: Smith

first: D

last: Dijk


title: Whole-transcriptome gene expression profiling in TRPC1-silenced cells

first: Cigdem

last: Selli

address: Little France Crescent

department: Centre for Reproductive Health

institute: Queen's Medical Research Institute

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

overall_design: Refer to individual Series


title: Properties of STAT1 and IRF1 Enhancers and the Influence of SNPs

city: Toronto

first: Rod

last: Bremner

state: ON

address: 600 University Ave

department: Lunenfeld-Tanenbaum Research Institute

institute: Mount Sinai Hospital

type: Genome binding/occupancy profiling by genome tiling array

first: R

first: Z

last: Xu

first: T

last: Yu

first: K

last: Huang

first: M

last: Hassan


title: Effect of Mut heterozygosity in skeletal muscle gene expression

first: Grace

last: Daher

address: 1 Joslin Place

institute: Joslin Diabetes Center

summary: Branched-chain amino acids (BCAA) have emerged as predictors of type 2 diabetes (T2D). However, their potential role in the pathogenesis of insulin resistance and T2D remains unclear. By integrating data from skeletal muscle gene expression and metabolomic analyses, we demonstrate evidence for perturbation in BCAA metabolism and fatty acid oxidation in skeletal muscle from insulin-resistant humans. Experimental modulation of BCAA flux in cultured cells alters fatty acid oxidation in parallel. Furthermore, heterozygosity for the BCAA metabolic enzyme methylmalonyl-CoA mutase (MUT) alters muscle lipid metabolism in vivo, resulting in increased muscle triacylglycerol (TAG) accumulation and increased body weight after high-fat feeding. Together, our results demonstrate that impaired muscle BCAA catabolism may contribute to the development of insulin resistance by reducing fatty acid oxidation and increasing TAG accumulation.

overall_design: 5-week-old Mut+/+ and Mut+/- male mice were fed a high-fat diet with 45% kcal from fat for 4 months. Mice were fasted overnight prior to sacrifice and quadriceps muscle was flash frozen in liquid nitrogen.

first: Carles

last: Lerin

first: Charles

last: Venditti

first: Mary

middle: E

last: Patti


title: Identification of Chd7 and Top2b regulated genes in cerebellar granule neurons

status: Public on Jan 20 2017

city: Heidelberg

first: Haikun

last: Liu

address: INF 581

institute: DKFZ

summary:
We performed array-based expression profiling to determine genes regulated by Chd7 and Top2b in CGNs. Our data show Chd7 and Top2b coregulate a common set of neuronal genes.
Furthermore, we compared the gene expession in proliferating and postmitotic granule cells.

overall_design: Three independent expesssion profiling. Two conditions for each.

first: Weijun

last: Feng

first: Daisuke

last: Kawauchi


title: Expression data from bone marrow and fetal liver of Col18-wt and Col18-KO mice

status: Public on Jan 22 2017

city: Oulu

first: Valerio

last: Izzi

state: Select a State or Province

address: Aapistie 7A

country: Finland

institute: University of Oulu

summary: Perturbations in the mechanisms controlling hematopoietic stem cells (HSCs) quiescence are believed to be at the roots of leukemic transformation. Through its ability to seize growth factors, provide docking to HSCs and modulate cell-to-cell signaling, the extracellular matrix (ECM) has been variously involved in HSCs quiescence and malignant transformation. In this context, different collagens (including Collagen VI and X) have been demonstrated to regulate HSCs growth and differentiation. Different reports suggest that Collagen XVIII (Col18), a member of the multiplexins collagen family, could play similar roles in maintaining HSCs and, potentially, in leukemic transformation, though any knowledge about its actual involvement in hematopoiesis is still lacking. Here we show that Col18 is needed to keep HSCs quiescent, and that its lack increases the risk of hematological neoplasms. We found that mice lacking Col18, in fact, have increased frequency of HSCs in both fetal liver and adult bone marrow, with a significant accumulation of myeloid precursors in the hematopoietic niches and of mature and immature myeloid cells in the blood. Along with hematopoietic deregulation, mice lacking Col18 showed a significant increase in the development of spontaneous lymphomas, a genetic predisposition to leukemic transformation, and lack of cell-to-ECM adhesion. We also confirmed that, in leukemic patients, Col18 is downregulated through genetic and epigenetic mechanisms and that such a downregulation decreases survival and contributes to a poorer prognosis. Our results demonstrate that Col18 is necessary to keep HSCs quiescent and to prevent excessive myeloid growth, and that alterations in its expression within the hematopoietic niche are likely to facilitate leukemic transformation and affect life expectancy of patients.

overall_design: Total RNA was isolated from E14.5 fetal liver (FL) or adult (3-months-old) bone marrow (BM) of mice lacking Col18a1 (Col18-wt) or wild-type (Col18-wt) littermates. Samples from Col18-wt and Col18-KO FL and BM were pooled in pairs (2 littermates/sample) before RNA extraction, and two independent replicates per genotype were prepared for each tissue before hybridization to Affymetrix Mouse Genome 430.2 array.

first: V

last: Pihlajaniemi


title: Protein abundance of AKT and ERK pathway components governs cell-type-specific regulation of proliferation

city: Lübeck

first: Hauke

last: Busch

state: Schleswig-Holstein

address: Ratzeburger Allee 160

department: Lübeck Institute of Experimental Dermatology

institute: University of Lübeck

summary: Activation of the AKT and ERK signaling pathway is a major contributor to cell proliferation. However, the integrated regulation of this multistep process, involving signal processing, cell growth and cell-cycle progression, is poorly understood. Here we study three cell types of hematopoietic origin, in which AKT and ERK signaling is triggered by erythropoietin (Epo). We find that the different cell types exhibit distinct proliferative responses, despite sharing the molecular network for pro-proliferative signaling. Iterating quantitative experiments and mathematical modeling, we show that the cell-type-specific regulation of proliferation emerges from two sources: (1) the protein abundance patterns of signaling components that cause differential flow of signals along the AKT and ERK pathways, and (2) the differential impact of the downstream regulators for protein synthesis and for cell-cycle progression on proliferation. Our integrated mathematical model of Epo-driven proliferation explains cell-type-specific effects of targeted AKT and ERK inhibitors and correctly predicts whether their combined application results in synergy.

overall_design: EpoR receptor as well as EpoR and Pten overexpressing BaF3 cells were growth factor deprived for 5 h and resuspended in RPMI supplemented with 1mg/ml BSA. Cells were stimulated with 1U/ml Epo and RNA was extracted at 0, 1, 2, 3, 4, 5, 7 and 18.5 hours after stimulation using the RNeasy Mini Plus Kit (Qiagen, Hilden, Germany).

first: Lorenz

last: Adlung

first: Sandip

last: Kar

first: Marie-Christine

last: Wagner

first: Bin

last: She

first: Jie

last: Bao

first: Susen

last: Lattermann

first: Melanie

last: Boerries

first: Jens

last: Timmer

first: Marcel

last: Schilling

first: Thomas

last: Höfer

first: Ursula

last: Klingmüller


title: Effect of Collagen Peptide-containing Diet on Hepatic Gene Expressions in Mouse

status: Public on Jan 17 2017

city: Aomori

first: Yuji

last: Nakai

state: Aomori

address: 2-1-1, Yanagawa

department: Institute of Regional Innovation

institute: Hirosaki University

summary: Ingestion of collagen peptide elicits beneficial effects on the body. Improvement of blood lipid is one of the effects, but its mechanism remains unclear. Male BALB/cCrSlc mice were bred with the AIN-93M diet containing 14% casein or AIN-93M-based low-protein diet containing 10% casein or diet containing 6% casein+4% collagen peptide (n=12/group) for 10 weeks．Total, free, and esterified cholesterol levels in the blood decreased in the collagen peptide group. DNA microarray analysis of the liver revealed that expression of the genes related to lipid metabolic process, such as PPAR signaling pathway and fatty acid metabolism, increased in the collagen peptide group compared to the 10% casein group. In contrast, expression of the genes related to unfolded protein response (UPR) and protein level of phospho-IRE1 decreased. Our data suggest that lipid metabolism in the liver was altered by collagen ingestion, which probably results in the decreased levels of blood cholesterol.

overall_design: Male 6-week-old BALB/cCrSlc mice were purchased from Japan SLC, Inc. (Shizuoka, Japan) and acclimatized to breeding conditions for 1 week in the laboratory animal facilities of Rakuno Gakuen University. They were divided into three groups (12 mice per group) based on body weight so that the average body weight did not differ significantly among groups. The mice were individually housed under conventional conditions (20±2°C, 12 h light/12 h dark cycle) with free access to water and diet. The basic powder diet AIN-93M-based low-protein diets containing 10% casein (10C) or 6% casein plus 4% collagen peptide (fish-derived, MW 4,000~6,000, Nippi Inc., Tokyo, Japan) (6C+4CP) were prepared by Oriental Yeast Co., Ltd. (Tokyo, Japan). Cornstarch was used to compensate for the decreased protein in the low-protein diets. Body weight, food and water intake were measured once a week.  After 10 weeks of the breeding, sampling was performed in the morning after starvation for 3 h. After anesthesia with 50mg/kg sodium pentobarbital, blood was collected from the right ventricle with a heparinized syringe, and plasma was stored at -80°C. Three mice of medium food efficiency (weight gain/food intake) were selected in each group for further analysis. Whole liver was removed and a portion of the first leaf (ca. 5 × 5 × 3 mm) was kept in RNAlater (Ambion, Austin, TX, USA) to isolate total RNA.   This study was conducted in accordance with the Act on Welfare and Management of Animals in Japan (Act No. 105 of October 1, 1973; partly revised on June 22, 2005), the Standards Relating to the Care and Management of Laboratory Animals and Relief of Pain (Notice No. 88 of the Ministry of the Environment, dated April 28, 2006), and the Guidelines for Methods of Animal Disposition Procedures (Prime Minister’s Office Notification No. 40, dated July 4, 1995; partly revised on November 12, 2007: Notice No. 105 of the Ministry of the Environment). The study protocol was approved by the Ethics Committee of Rakuno Gakuen University (No. VH23A8).

first: Chisa

last: Tometsuka

first: Yoh-ichi

last: Koyama

first: Tomoko

last: Ishijima

first: Tsudoi

last: Toyoda

first: Miki

last: Teranishi

first: Kazushige

last: Takehana

first: Keiko

last: Abe


title: Antidyskinetic effects of MEK inhibitor are associated with multiple neurochemical alterations in the striatum of hemiparkinsonian rats

status: Public on Jan 18 2017

city: Wuhan

first: Guiqin

last: Chen

state: Huebei

address: 277 Jiefang Avenue

department: Department of Neurology

institute: Union Hospital, Tongji Medical College, Huazhong University of Science and Technology

summary: L-DOPA-induced dyskinesia (LID) represents one of the major problems of the long-term therapy of patients with Parkinson's disease (PD). Although the pathophysiologic mechanisms underlying LID are not completely understood, activation of the extracellular signal regulated kinase (ERK) is recognized to play a key role. ERK is phosphorylated by mitogen-activated protein kinase kinase (MEK), and thus MEK inhibitor can prevent ERK activation. Here the effect of the MEK inhibitor PD98059 on LID and the associated molecular changes were examined. Rats with unilateral 6-OHDA lesions of the nigrostriatal pathway received daily L-DOPA treatment for three weeks, and abnormal involuntary movements (AIMs) were assessed every other day. PD98059 was injected in the lateral ventricle daily for 12 days starting from day 10 of L-DOPA treatment. Striatal molecular markers of LID were analyzed together with gene regulation using microarray. The administration of PD98059 significantly reduced AIMs. In addition, ERK activation and other associated molecular changes including ΔFosB were reversed in rats treated with the MEK inhibitor. PD98059 induced significant up-regulation of 418 transcripts and down-regulation of 378 transcripts in the striatum. Tyrosine hydroxylase (Th) and aryl hydrocarbon receptor nuclear translocator (Arnt) genes were down-regulated in lesioned animals and up-regulated in L-DOPA-treated animals. Analysis of protein levels showed that PD98059 reduced the striatal TH. These results support the association of p-ERK1/2, ΔFosB, p-H3 to the regulation of TH and ARNT in the mechanisms of LID, and pinpoint other gene regulatory changes, thus providing clues for identifying new targets for LID therapy.

overall_design: 15 samples were analyzed in the microarray. There were 3 samples in each group (Normal Group, PD group, LID group, LID+Vehicle froup, LID+PD98059)

first: Shuke

last: Nie

first: Chao

last: Han

first: Kai

last: Ma

first: Yan

last: Xu

first: Zhentao

last: Zhang

first: Stella

last: Papa

first: Xuebing

last: Cao


title: Integrated functional genomics and craniofacial morphogenesis within the FaceBase Consortium: Alk5 mutant

status: Public on Jan 13 2017

city: Los Angeles

first: Michael

last: Kesling

address: 2250 Alcazar Street

institute: University of Southern California

summary: Congenital malformations in facial bones significantly impact the overall representation of the face. Establishing correlations between gene expression and morphogenesis of craniofacial structures may lead to new discoveries of molecular mechanisms of craniofacial development. Thus in the present investigation, we will generate gene expression profiles of facial bones at embryo stage 14.5 to establish their roles in regulating craniofacial development.

overall_design: To perform global gene expression profiling analysis of mandible and maxilla development and integrate these datasets with cell lineage and quantitative 3D dynamic imaging analyses. In collaboration with the ontology group within the FaceBase consortium, we will define anatomical landmarks and morphometric parameters of the developing mandible and maxilla. Wnt1cre;Alk5fl/+ mice were mated with Alk5fl/fl mice and pregnant females were sacrificed at embryonic day 14.5 (E14.5), with observance of a vaginal plug denoting E0. Mutant embryos were identified by the presence of cleft palate and calvarial defect. The mandible and maxilla were dissected away from mutant embryos and control litter mates, then each mandible and maxilla was divided into its distal and proximal ends.

first: Yang

last: Chai

first: Carolina

last: Parada

first: Alexandre

last: Grimaldi

first: Thach

last: Ho

first: Jill

last: Harunaga

first: Bridget

last: Samuels

first: Vasu

last: Punj


title: Enhanced functional recovery from spinal cord injury in aged mice after stem cell transplantation through HGF induction

city: Tokyo

first: Morito

last: Takano

address: 35 Shinanomachi, Shinjuku-ku

department: Orthopaedic Surgery

institute: Keio University

summary: The number of elderly patients with spinal cord injury (SCI) is increasing worldwide, representing a serious burden for both the affected patients and the community. Previous studies have demonstrated that neural stem cell (NSC) transplantation is an effective treatment for SCI in young animals. Here we show that NSC transplantation is as effective in aged mice as it is in young mice, even though aged mice exhibit more severe neurological deficits after SCI. NSCs grafted into aged mice exhibited better survival than did those grafted into young mice. Furthermore, we show that the neurotrophic factor HGF plays a key role in the enhanced functional recovery after NSC transplantation observed in aged mice with SCI. The unexpected results of the present study suggest that NSC transplantation is a potential therapeutic modality for SCI, even in elderly patients.

overall_design: Injured and naive mice were anesthetized and transcardially perfused with heparinized saline (5 U/ml) 9 days after injury (n=3 each). Dissected segments of the spinal cord at the Th9 level underwent expression profiling by array.

first: Narihito

last: Nagoshi

first: Shinsuke

last: Shibata

first: Akimasa

last: Yasuda

first: Satoshi

last: Nori

first: Osahiko

last: Tsuji

first: Hayao

last: Ebise

first: Keisuke

last: Horiuchi

first: Hideyuki

last: Okano

first: Masaya

last: Nakamura


title: Slug-induced miR-137 expression contributes to non-small cell lung cancer progression

status: Public on Jan 01 2017

city: Taipei

first: Jin-Yuan

last: Shih

address: #7, Chung-Shan South Road,

department: Internal Medicine

institute: National Taiwan University Hospital

summary: The epithelial-mesenchymal transition (EMT) regulator Slug has multifaceted roles in controlling lung cancer progression, but the downstream targets and underlying mechanisms of Slug remain undetermined. The miRNAs downstream of Slug in lung cancer cells were examined using Illumina bead arrays and TaqMan low-density arrays.

overall_design: The Slug-overexpressing cells (CL1-0-Slug-4) and control cells (CL1-0-mock) were selected with 500ug/ml G418 in CL1-0 cells.  We tried to compare the Slug-expressing profiles with the negative control to identify the possible mechanisms of Slug-regulated microRNA in lung cancer cells.

first: Tzu-Hua

last: Chang

first: Meng-Feng

last: Tsai

first: Shang-Gin

last: Wu

first: Yi-Nan

last: Liu

first: Yih-Leong

first: Sung-Liang

last: Yu

first: Hsing-Chen

first: Shr-Uen

last: Lin

first: Yen-Wei

last: Chen

first: Po-Yen

last: Kuo

first: Pan-Chyr

last: Yang


title: Male and female mouse primary astrocytes stably transfected with Cdca7l

status: Public on Jan 15 2017

city: Frederick

first: Karlyne

last: Reilly

address: West 7th St at Fort Detrick, PO Box B

department: Mouse Cancer Genetics Program

institute: National Cancer Institute, Center for Cancer Research

summary: Cdca7l acts as a male-specific oncogene in astrocytoma and glioblastoma, and can transform primary astrocyte growth in soft agar. We stably overexpressed Cdca7l in mouse primary astrocytes and compared gene expression to primary astrocytes expressing empty vector control in male and female cell to identify gene expression differences between male and female cells and between Cdca7l-overexpressing and normal primary astrocytes.

overall_design: Independent primary astrocyte isolates were stably transfected with either Cdca7l or an empty vector control. 4-5 biological replicates were used for each of 4 groups: C57BL/6J (B6) male astrocytes, C57BL/6J (B6) female astrocytes, 129S4/SvJae (129) male astrocytes, and 129S4/SvJae (129) female astrocytes

first: Min-Hyung

last: Lee


title: Complementary critical functions of Zfy1 and Zfy2 in mouse spermatogenesis and reproduction.

status: Public on Jan 12 2017

city: tokyo

first: Takashi

last: Nakasuji

address: 1-5-45 yushima bunkyo

institute: Tokyo Medical and Dental University

summary: The mammalian Y chromosome plays a critical role in spermatogenesis. However, the exact functions of each gene in the Y chromosome have not been completely elucidated, partly owing to difficulties in gene targeting analysis for the Y chromosome. Zfy was first proposed to be a sex determination factor, but its function in spermatogenesis has been recently elucidated. Nevertheless, Zfy gene targeting analysis has not been performed thus far. Here, we adopted the highly efficient CRISPR/Cas9 system to generate individual Zfy1 or Zfy2 knockout (KO) mice, and Zfy1 and Zfy2 double knockout (Zfy1/2-DKO) mice. While individual Zfy1 or Zfy2-KO mice did not show any significant phenotypic alterations in fertility, Zfy1/2-DKO mice were infertile and displayed abnormal sperm morphology, fertilization failure, and early embryonic development failure. Mass spectrometric screening, followed by confirmation with western blot analysis, showed that PLCZ1, PLCD4, PRSS21, and HTT protein expression was significantly deceased in spermatozoa from Zfy1/2-DKO mice compared with those from wild type mice. These results are consistent with the phenotypic changes seen in the double mutant mice. Collectively, our strategy and findings revealed that Zfy1 and Zfy2 have redundant functions in spermatogenesis, facilitating a better understanding of fertilization failure and early embryonic development failure.

overall_design: Testes were prepared from wild type and Zfy1, 2 double knockout mice for RNA extraction and hybridization on Affymetrix microarrays.

first: Hiroshi

last: Asahara


title: Expression data from mouse white adipose tissue lacking CNOT3, a core subunit of the CCR4-NOT complex

city: Onna

first: Toru

last: Suzuki

state: Okinawa

address: 1919-1 Tancha

institute: Okinawa Instutue of Science and Technology Graduate University

summary:
mRNA degradation critically contributes to tissue development and function as well as transcription. The CCR4-NOT complex serves as a major deadenylase that initiates mRNA degradation.
We used microarrays to identify deregulated genes in the white adipose tissues lacking CNOT3, a core subunit of the CCR4-NOT complex.

overall_design: Adipose tissue-specific CNOT3 knockout mice were generated by expressing Cre recombinase under the control of Adiponectin promoter. White adipose tissues from control and CNOT3 knockout mice were used for RNA extraction and hybridization on Affymetrix microarrays.

first: Li

last: Xue

first: Chisato

last: Kikuguchi


title: Astrocytic calcium waves signal brain injury to neural stem and progenitor cells

status: Public on Jan 11 2017

city: Frankfurt am Main

first: Stefan

last: Momma

address: Heinrich-Hoffmann-Str. 7

department: Neurological Institute (Edinger Institute)

institute: University Hospital Frankfurt am Main

summary: Gene expression patterns in the SVZ, 48 h after an ischemic lesion caused by permanent middle cerebral artery occlusion (MCAO)

overall_design: Adult male C57/BL6 mice were subjected to middle cerebral artery occlusion. After 48h, mice were killed and the subventricular zone ipsilateral to the lesion (and sham-surgery controls) were dissected out and RNA extracted for RNA microarray analysis

first: Claudia

last: Döring


title: Ring1A and Ring1B maintain murine MOZ-TIF2 AML stem cells by inhibiting expression of Glis2

status: Public on Jan 06 2017

city: Cho-ku

first: Emi

last: Takamatsu-Ichihara

state: Tokyo

address: 5-1-1, Tsukiji

institute: National Cancer Center Research Institute

summary: Eradication of chemotherapy-resistant leukemia stem cells is expected to improve treatment outcomes in patients with acute myelogenous leukemia (AML). In a mouse model of AML expressing the MOZ-TIF2 fusion, we found that Ring1A and Ring1B, components of Polycomb repressive complex 1, play crucial roles in maintaining AML stem cells. Deletion of Ring1A and Ring1B (Ring1A/B) from MOZ-TIF2 AML cells diminished self-renewal capacity and induced the expression of numerous genes including Gli-similar 2 (Glis2). Overexpression of Glis2 caused MOZ-TIF2 AML cells to differentiate into mature cells, whereas Glis2 knockdown in Ring1A/B-deficient MOZ-TIF2 cells inhibited differentiation. Thus, Ring1A/B regulates and maintains AML stem cells in part by repressing Glis2 expression, which promotes their differentiation. These findings provide new insights into the mechanism of AML stem cell homeostasis and reveal novel targets for cancer stem cell therapy.

overall_design: To identify the target genes implicated in the regulation of AML stem cells by PRC1, we performed gene expression profiling in Ring1A-/-;Ring1Bf/f and Ring1A-/-;Ring1BΔ/Δ MOZ-TIF2 cells. Ring1B was conditionally deleted by treating the cells with 4-OHT for 48h or 7days.

first: Haruko

last: Shima

first: Issay

last: Kitabayashi


title: The effect of c-Abl inhibitor AMN on the induce expression profile of IFN response genes from MEFs

city: Beijing

first: yan

last: cui

state: beijing

address: 27 Taiping Road

department: Department of Molecular Biology

institute: Beijing Institute of Biotechnology

summary:
MEFs were stimulated for 6 h with IFNa or IFNg after pretreatment with AMN107 or DMSO for at least 18 h.
We used microarrays to detail the global programme of gene expression of IFN-regulated genes

overall_design: MEFs were treated with or without AMN107, then were stimulated for 6 h with IFNa or IFNg. RNA extraction and hybridization on Affymetrix microarrays


title: Integrated functional genomics and craniofacial morphogenesis within the FaceBase Consortium: Alk5 and TGFBR2 mutants

first: Michael

last: Kesling

summary:
Congenital malformations in facial bones significantly impact the overall representation of the face. Establishing correlations between gene expression and morphogenesis of craniofacial structures may lead to new discoveries of molecular mechanisms of craniofacial development. Thus in the present investigation, we will generate gene expression profiles of facial bones at embryo stage 14.5 to establish their roles in regulating craniofacial development.

This SuperSeries is composed of the SubSeries listed below.

overall_design: To perform global gene expression profiling analysis of mandible and maxilla development and integrate these datasets with cell lineage and quantitative 3D dynamic imaging analyses. In collaboration with the ontology group within the FaceBase consortium, we will define anatomical landmarks and morphometric parameters of the developing mandible and maxilla. Wnt1cre;Alk5fl/+ mice were mated with Alk5fl/fl mice and pregnant females were sacrificed at embryonic day 14.5 (E14.5), with observance of a vaginal plug denoting E0. Mutant embryos were identified by the presence of cleft palate and calvarial defect. The mandible and maxilla were dissected away from mutant embryos and control litter mates, then each mandible and maxilla was divided into its distal and proximal ends. For the TGFBR2 mutant, essentially the same protocol was used except that Wnt1cre;Tgfbr2fl/+ mice were mated with Tgfbr2fl/fl mice.

first: Yang

last: Chai

first: Carolina

last: Parada

first: Alexandre

last: Grimaldi

first: Thach

last: Ho

first: Jill

last: Harunaga

first: Bridget

last: Samuels

first: Vasu

last: Punj