title: De novo generation of somatic stem cells from differentiated cells [pancreatic]

summary: To investigate the role of YAP/TAZ as factors able to convert differentiated cells into stem cells of the same tissue, we compared the expression profiles of pancreatic organoids (yDucts) obtained by doxycycline-inducible expression of YAP in pancreatic acini with original acini and native ducts (Ducts).

overall_design: We collected RNA from Ducts, yDucts, and acini. Samples were then processed for total RNA extraction and hybridization on Affymetrix microarrays. Four biological replicas (A, B, C, D) were used for each sample, for a total of 12 samples.


title: Expression data from colorectal biopsy samples - adenomas or normal mucosae

status: Public on Aug 26 2016

city: Paris

first: Pierre

last: de la Grange

address: 29, rue du Faubourg Saint-Jacques

department: Paris Biotech Santé

country: France

institute: GenoSplice technology

summary: We showed that a large number of genes and exons were deregulated in colorectal adenomas in comparison with colorectal normal mucosa.

overall_design: 24 colorectal adenoma samples and a pool of 2 colorectal normal mucosae were analysed. We generated a comparison between adenomas and normal mucosa.

first: Marine

last: Pesson

first: Alain

last: Volant

first: Kilian

last: Trillet

last: De La Grange

first: Mélanie

last: Daoulas

first: Michel

last: Robaskiewicz

first: Gérald

last: Le Gac

last: Morel

first: Brigitte

last: Simon

first: Laurent

last: Corcos


title: C4b-binding protein protects beta-cells from islet amyloid polypeptide induced cytotoxicity.

status: Public on Aug 25 2016

city: Lund

first: Petter

last: Storm

address: Sölvegatan 19, BMC A11

department: Developmental and Regenerative Neurobiology

country: Sweden

institute: Lund University

summary: Complement inhibitor C4b-binding protein (C4BP) is synthesized in liver and pancreas and composed of 7 identical alpha chains and one unique beta chain. We showed previously that C4BP binds islet amyloid polypeptide (IAPP) and affects fibril formation in vitro. Now we found that polymeric C4BP inhibited lysis of human erythrocytes incubated with monomeric IAPP while no erythrocyte lysis was observed after incubation with preformed IAPP fibrils. In contrast, monomeric alpha chain of C4BP had significantly reduced activity. Further, addition of monomeric IAPP to a rat insulinoma cell line (INS-1) resulted in decreased cell viability, which was restored in the presence of physiological concentrations of C4BP. Accordingly, addition of C4BP rescued the ability of INS-1 cells and isolated rat islets to respond to glucose stimulation with insulin secretion, which was impaired in the presence of IAPP alone. C4BP was internalized together with IAPP into INS-1 cells and therefore we aimed to study its effect on gene expression. Pathway analyses of mRNA expression microarray data indicated that cells exposed to C4BP and IAPP in comparison to IAPP alone increased expression of genes involved in cholesterol synthesis. Depletion of cholesterol through methyl-β-cyclodextrin or cholesterol oxidase abolished the protective effect of C4BP on IAPP cytotoxicity of INS-1 cells. Also, inhibition of phosphoinositide 3-kinase but not NF-κB had a similar effect. Taken together, one of the mechanisms by which C4BP protects beta-cells from IAPP cytotoxicity is by enhancing cholesterol synthesis.

overall_design: The INS-1 cells were grown as 5 separate clones for 10 passages before plating in a 12-well plate (Nunc) at 100.000 cells per well and grown in complete RPMI 1640 medium to 70% confluency for approximately 48 h. The cells were then challenged by adding 77 μM monomeric IAPP alone or together with C4BP (0.6 μM). DMSO (1%) used as solvent for IAPP as well as C4BP (0.6 μM) alone were used as controls. RNA was extracted after 10h incubation and analysis carried out using Rat Gene 2.0 array chip (Affymetrix).

first: Anna

last: Blom


title: Transcriptomes of mouse PGCLCs isolated from 6-day culture embryoid bodies were compared with transcriptomes of their precur cells (ESCs, iPSCs, and EpiLCs) and E12.5 in vivo mouse PGCs

status: Public on Aug 22 2016

city: Charlestown

first: Toshihiro

last: Shioda

state: MA

address: Building 149 - 7th Floor, 13th Street

department: Center for Cancer Research

country: USA

institute: MGH Cancer Center

summary: Transcriptomes of mouse E12.5 primordial germ cells (PGCs), primordial germ cell-like cells (PGCLCs) isolated from 6-day culture embryoid bodies,  and the precursor pluripotent stem cells [embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs)] and epiblast-like cells (EpiLCs)

overall_design: Total RNA was isolated from FACS-enriched, SSEA1+/CD61+ double-positive PGCs and PGCLCs. RNA was also isolated from ESC, iPSC, and EpiLC cultured without enrichment. Transcriptomes were determined using Affymetrix microarray.

first: Norikatsu

last: Miyoshi

first: Jente

middle: M

last: Stel

first: Haley

last: Ellis

first: Keiko

first: Toshi


title: Gene expression profiling of mice given orally a supplement with special amino acid composition of Vespa larval saliva origin (DW vs CAAM)

status: Public on Sep 06 2016

city: Kawasaki

first: Fumika

last: SHINOZAKI

address: 3-25-13 Tonomachi, Kawasaki-ku

country: Japan

institute: Kanagawa Institute of Industrial Science and Technology

summary: VAAM stands for an amino acid mixture simulating the composition of Vespa, a hornet larval saliva. We conducted a comparative study on metabolism-regulatory roles of VAAM, casein-simulating amino acid mixture (CAAM), and pure water on murine hepatic and adipose tissue transcriptomes. Mice were orally fed VAAM solution ( 0.675 g/ kg BW = 2% of food-derived amino acids = 0.38% of total food energy/ day), CAAM solution ( 0.675 g / kg BW/ day) or water under ad libitum for five days. Hepatic transcriptome comparison of VAAM, CAAM and water-treated groups revealed a VAAM-specific regulation of the metabolic pathway, i.e., the down-regulation of glycolysis and fatty acid oxidation, and up-regulation of poly unsaturated fatty acid synthesis and glycogenic amino acids utilization in TCA cycle. Similar transcriptomic analysis of white and brown adipose tissues (WAT and BAT) suggested the up-regulation of phospholipid synthesis in WAT and the negative regulation of cellular processes in BAT. Because these coordinated regulations of tissue transcriptomes implicated the presence of upstream signaling common to these tissues, we conducted Ingenuity Pathways Analysis of these transcriptomes with the results that estrogenic and glucagon signals seemed to be activated in liver and WAT as well as beta-adrenergic signaling did in the three tissues by administration of VAAM. Our data provide a clue to understanding the role of VAAM in metabolic regulation of multiple tissues.

overall_design: Mice were divided randomly into three groups, VAAM, CAAM or water administered group. VAAM, CAAM or water was orally administrated five times once a day using feeding tube. The dosage of 1.8%VAAM, 1.8%CAAM or water was 37.5 microliter per gram of body weight. On day of last administration, food was removed and mice were moved to clean cages at 8:00. The last administrations started at 10:00. At 4 hours later after last administration, mice were sacrificed by cervical dislocation to collect blood, liver, white adipose tissue (WAT) and brown adipose tissue (BAT). Small hepatic pieces were immersed into RNAlater. WAT and BAT were frozen immediately after extraction using liquid nitrogen. All samples were extracted total RNA and hybridized on Affymetrix microarrays.


title: Hepatic Gene Expression Changes in Diethynitrosamin-initiated and Cholic Acid promoted tumors

status: Public on Aug 10 2016

city: Kansas City

first: Udayan

last: Apte

state: KS

address: 3901 Rainbow Blvd

department: Pharmacology, Toxicology and Therapeutics

institute: University of Kansas Med Center

summary: Mice were fed with either normal diet (ND), 0.2% cholic acid diet (0.2%CA), DEN treated and fed ND or DEN treated and fed 0.2%CA diet. DEN was treated at 15 microgram/kg body weight at postnatal day 15. Diets were fed for two months starting 8 months of age till 10 months of age. Livers were collected at10 months of age, Total RNA was isolated and used for microarray experiments.

overall_design: 4 groups [ND, 0.2%CA, DEN+ND and DEN+0.2%CA], pooled livers from 3-5 mice


title: Histone deacetylase 3 is essential for pregnancy

status: Public on Sep 01 2016

city: Columbia

first: Jae-Wook

last: Jeong

state: MO

address: 1030 Hitt Street

department: Obstetrics, Gynecology and Women's Health

institute: University of Missouri

summary:
HDAC3 is necessary for implantation and decidualization, and its defects that may be a cause of reproductive failure.
We used microarrays to detail the mechanism underlying HDAC3 loss for reproductive failure

overall_design: Uteri of Hdac3 f/f and Hdac3 d/d mice were selected at 6 weeks of age for RNA extraction and hybridization on Affymetrix microarrays.

first: Tae

middle: H

last: Kim


title: Expression of rat hepatocytic progenitor cells with and without hepatic Thy1-positive cells in retrorsine/partial hepatectomy treated rats models.

status: Public on Aug 14 2016

city: Sapporo

first: Norihisa

last: Ichinohe

state: Hokkaido

address: South-1, West-17, Chuo-ku,

department: Department of Tissue Development and Regeneration

institute: Sapporo Medical University School of Medicine

summary:
We found that the transplantation of Thy1+ cells transiently increased the liver mass by expanding resident small hepatocy-like progenitor cells(SHPCs).
We used microarrays to detail the gene expression of receptors of growth factors of SHPCs clusters with and without Thy1+ cells transplantation.

overall_design: SHPCs clusters were selected by micro-dissected from Ret/PH livers for RNA extraction and hybridization on Affymetrix microarrays.

first: N


title: Expression data from control and Med12-deficient hematopoietic stem cells and progenitors

city: New York

first: Beatriz

last: Aranda-Orgilles

address: 522 First Avenue

institute: NYU School of Medicine

summary:
Hematopoietic stem cells and progenitors from controls and Med12Flox; mxCre mice treated with pI:pC 4 days afters injection were sorted and Micrroarray Affymetrix mouse 430.2 platform.
Results provide insight into the gene signatures regulated by Med12 that are essential for the homeostasis of the hematopoietic system.

overall_design: Microarrays we used to characterize the gene expression programs regulated by Med12 and identified down-regulated signatures

first: Aifantis

last: Iannis

first: Aranda-Orgilles

last: Beatriz


title: Comparison between Nestin+ and Nestin- Ptch1 deficient GNPs

status: Public on Aug 09 2016

city: Philadelphia

first: Zeng-jie

last: Yang

state: Pennsylvania

address: 333  Cottman Avenue

department: Cancer Biology Program

institute: Fox Chase Cancer Center

summary: The intermediate filament protein Nestin serves as a biomarker for stem cells and has been used to identify subsets of cancer stem-like cells. However, the mechanistic contributions of Nestin to cancer pathogenesis are not understood. Here we report that Nestin binds the hedgehog pathway transcription factor Gli3 to mediate the development of medulloblastomas of the hedgehog subtype. In a mouse model system, Nestin levels increased progressively during medulloblastoma formation resulting in enhanced tumor growth. Conversely, loss of Nestin dramatically inhibited proliferation and promoted differentiation. Mechanistic investigations revealed that the tumor-promoting effects of Nestin were mediated by binding to Gli3, a zinc finger transcription factor that negatively regulates hedgehog signaling. Nestin binding to Gli3 blocked Gli3 phosphorylation and its subsequent proteolytic processing, thereby abrogating its ability to negatively regulate the hedgehog pathway. Our findings show how Nestin drives hedgehog pathway-driven cancers and uncover in Gli3 a therapeutic target to treat these malignancies.

overall_design: Nestin+ and Nestin- GNPs (granule neuron precursors) were purified from Nestin-CFP/Math1-Cre/Ptch1-loxp cerebella at postnatal day 4 by FACs, and total RNA from these two cell populations were extracted, and then labeled and hybridized to Affymetrix Mouse Genome 430 2.0 arrays.


title: Microarray data of epidermal basal cells from ventral or dorsal skin of virgin and pregnant mice

status: Public on Aug 30 2016

city: Bunkyo-ku

first: Fumiko

last: Toyoshima

state: Tokyo

address: 1-5-45 Yushima

department: Medical Research Laboratory

institute: Institute of Science Tokyo

summary: To identify genes expressed predominantly in the ventral skin epidermal basal cells of pregnant mice, we performed DNA microarray analysis by using FACS-purified epidermal basal cells from ventral skin at 0 and 16 dpc, and dorsal skin at 16 dpc.

overall_design: The ventral or dorsal skin tissues were isolated from 8-12-week-old C57BL/6 virgin or pregnant (at 16 dpc) female mice. The alpha-6-integrin+ epidermal basal cells were FACS-purified from the isolated skin tissues. Total RNA was isolated from the basal cells and subjected to Affymetrix microarray using GeneChip 3'IVT Expression Kit. The experiments were performed twice.

first: Ryo

last: Ichijo


title: Microarray data of epidermis and dermis from virgin and pregnant mice

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

overall_design: Refer to individual Series


title: Expression profiling of total salivary gland from NOD.H-2h4 mice  with CD40L blockade

status: Public on Aug 29 2016

city: Gaithersburg

first: Jingya

last: Wang

state: Maryland

address: 1 medimmune way

department: Respiratory, Inflammation and Autoimmunity

institute: Medimmune

summary: Autoantibodies that arise in autoimmunity can be present years to decades prior to the onset of disease manifestations. This suggests that the initial autoimmune trigger involves a peripheral lymphoid component, which then drives disease pathology in local tissues later in life.  To explore the impact of early peripheral immune dysregulation on the progression of Sjögren’s Syndrome, we blocked the CD40-CD40L pathway in young female NOD.H-2h4 mice at 4 weeks of age with a single injection of anti-CD40L antibody, and collected total salivary gland at the age of week 8, 16 and 24. RNA was extracted and submitted to transcriptome profiling using Affymetrix microarray.

overall_design: NOD.H-2h4 female mice were treated intra-peritoneally at 4 weeks of age with a single injection of anti-CD40L or human IgG1 isotype control  mAb at 20 mg/kg. Total salivary gland was collected at week 8, week 16 and week 24. RNA was extracted and transcriptome profiling performed using Affymetrix Mouse Genome 430 2.0 Array

first: Rachel

last: Ettinger

first: Mahmoud

last: Tamer


title: Comparison of transcriptomes of mouse cumulus cells collected from mice before and after 6-h of hCG priming.

status: Public on Aug 01 2016

city: Nanjing

first: You-Qiang

last: Su

state: Jiangsu

address: 140 Hanzhong Road

department: State Key Laboratory of Reproductive Medicine

country: China

institute: Nanjing Medical University

summary:
We sought to identify genes that are regulated by the ovulatory signals in mouse cumulus cells.
We compared the transcriptomes between cumulus cells colected from mice before (hCG-0h) and after 6 h (hCG-6h) of hCG injection.

overall_design: 3 individual cumulus cell samples of hCG-0h and hCG-6h were collected and subjected to microarray study. Copmarison was done between hCG-0h and hCG-6h groups.


title: Changes in global gene expression in SIN1 knock-out murine epithelial fibroblasts

city: Piscataway

first: Estela

last: Jacinto

state: NJ

address: 683 Hoes Lane

department: Biochemistry and Molecular Biology

institute: Rutgers-Robert Wood Johnson Med School

summary:
RNA from wt and SIN1 knock-out MEF cell lines were compared
Using affymetrix murine gene chip, the effects of SIN1 ablation on global gene transcription were assessed

overall_design: RNA from wild type and SIN1 knock out cells was purified and differences in gene expression between the two sets. MEFs were derived from C57BL/6 (Jacinto et. al. Cell. 2006 Oct 6;127(1):125-37. Epub 2006 Sep 7

first: Matthew

last: Adlam


title: Defining memory-like CD8 T cells that respond to PD-1 therapy in chronic viral infection

status: Public on Aug 02 2016

city: Atlanta

first: Haydn

last: Kissick

state: Georgia

address: 1462 Clifton Rd

institute: Emory University

summary: Chronic viral infections are characterized by a state of CD8 T cell dysfunction termed exhaustion. A better understanding of the mechanisms that regulate CD8 T cell responses during chronic infection is required to improve immunotherapies that restore function in exhausted CD8 T cells. Here we identify a novel population of virus-specific CD8 T cells with a T follicular helper (Tfh)-like signature in mice chronically infected with lymphocytic choriomeningitis virus (LCMV). These Tfh-like CD8 T cells expressed the programmed cell death-1 (PD-1) inhibitory receptor but at the same time also expressed co-stimulatory molecules and had a gene signature that was related to CD8 T cell memory precursor cells and hematopoietic stem cells (HSC). These Tfh-like CD8 T cells acted as stem cells during chronic infection undergoing self-renewal and also differentiating into the terminally exhausted CD8 T cells that were present in both lymphoid and non-lymphoid tissues. The Tfh-like CD8 T cells were found only in lymphoid tissues and resided predominantly in the T cell zones along with naïve CD8 T cells. Interestingly, the proliferative burst after PD-1 blockade came almost exclusively from this Tfh-like CD8 T cell subset. Importantly, the transcription factor TCF1 played a cell intrinsic and essential role in the generation of Tfh-like CD8 T cells. Taken together, our study identifies Tfh-like CD8 T cells as the critical subset for maintaining the pool of virus-specific CD8 T cells during chronic infection and as the cells that proliferate after PD-1 blockade. These findings provide a better understanding of T cell exhaustion and have implications towards optimizing PD-1 directed immunotherapy.

overall_design: 8 samples isolated from CD8 T-cells in LCMV clone 13 GK1.5 infected mice (2 naïve, 3 CXCR5+Tim3-, 3 CXCR5-Tim3+) cells were analyzed

first: Rafi

last: Ahmed

first: Sejin

last: Im


title: Transcriptomic study of breast angiosarcomas induced by radiotherapy using formalin-fixed paraffin (FFPE) embedded tissues

status: Public on Aug 08 2016

first: Pierre

last: de la Grange

summary: A transcriptome signature which discriminate efficiently primary and radiation induced breast angiosarcomas can be generated from FFPE tumor samples.FFPE samples are good material to unlock relevant informations from tumors.

overall_design: The transcriptome of 35 FFPE breast angiosarcomas (10 primary and 25 radiation induced) were analysed using Affymetrix Human Exon 1.0 ST arrays according to the FFPE dedicated protocole from NuGEN and compared to paired fresh frozen samples previously analysed. FF Samples are also available in Array Express as E-MEXP-3252.

first: A

last: Almeida

first: P

first: B

last: Malfoy


title: Exploration of the genes affecting the compound acting against emphysema development in a mouse model of elastase-induced emphysema.

status: Public on Aug 24 2016

city: Tokushima

first: Hisashi

last: Nagamoto

address: 463-10 Kagasuno, Kawauchi-cho

institute: Otsuka Pharmaceutical Co., Ltd.

summary: In a mouse model of elastase-induced emphysema, the effect of tetomilast against the emphysema development observed in C57BL/6J (C57) could be also detected in phosphodiesterase (PDE) 4D(+/+) but not in PDE4B(+/+), PDE4B(-/-), and PDE4D(-/-) mice. Based on this result, we hypothesized that the difference in the efficacy of tetomilast among these strains of mice might result from the differences in the levels of the target molecules of tetomilast other than PDE4 in each mouse strain. To test this hypothesis, we used microarrays to compare the expression levels of genes in the lungs of each mouse strain. The expression profiling by array demonstrated that the levels of cyclin-dependent kinase inhibitor 1 (CDKN1a) in PDE4B(+/+), PDE4B(-/-), and PDE4D(-/-) were higher than those in C57 and PDE4D(+/+).

overall_design: Total RNAs were extracted from the lungs from naïve mice in each strain [C57, PDE4B(+/+), PDE4B(-/-), PDE4D(+/+), and PDE4D(-/)], and were used for microarray. In comparison with the expression levels of genes in C57, we retrieved the genes which expressed at the same levels in PDE4D(+/+), and at the different levels in PDE4B(+/+), PDE4B(-/-), and PDE4D(-/-).


title: Thymic XCR1+ dendritic cells undergo a functional maturation fundamentally similar to that of peripheral tolerogenic XCR1+ dendritic cells

city: MARSEILLE

first: Marc

last: DALOD

address: Parc Scientifique et Technologique de Luminy, 163 avenue de Luminy, Case 906, 13288 Marseille cedex 9

institute: CIML

summary: Dendritic cells (DC) play critical roles in central and peripheral T cell tolerance. DC found in the steady-state periphery undergo an homeostatic, tolerogenic, maturation that promotes interaction with naive T cells and induction of abortive responses. In contrast, thymic DC are thought to exist solely in an immature state. In this study, we show that XCR1+ thymic DC constitutively mature into a stage characterized by high levels of molecules involved in T cell activation. This unanticipated mature stage corresponded to a third of the XCR1+ thymic DC and fully accounted for their ability to cross-present self-antigens to developing T cells. Transcriptomic analysis of the XCR1+ DC found in thymus and steady-state periphery revealed that their maturation involves profound and convergent changes. Unexpectedly, maturation resulted in down-regulation of genes conferring their specific function on XCR1+ DC. Paradoxically, upon maturation, central and peripheral tolerogenic XCR1+ DC up-regulated many genes thought to drive pro-inflammatory T-cell responses. Thus, our results reveal that thymic XCR1+ DC undergo constitutive maturation and emphasize the common mechanisms operating for both central and peripheral tolerance induction by XCR1+ DC.

overall_design: DC were isolated from lymphoid organs as previously described (Vremec et al., 2000). DC subsets were sorted by flow cytometry according to the marker combinations described in the “characteristics: phenotype” field for each sample.

first: Laurence

last: Ardouin

first: Hervé

last: Luche

first: Frédéric

last: Montanana-Sanchis

first: Rabie

last: Chelbi

first: Sabrina

last: Carpentier

first: Samira

last: Tamoutounour

first: Sandrine

last: Henri

last: Dalod

first: Bernard

last: Malissen


title: Expression data from subsets of mouse spleen dendritic cells

status: Public on Jul 27 2016

city: Shanghai

first: Zhenhong

last: Guo

address: 800 Xiangyin Road

department: Department of Immunology

institute: Second Milirary Medical University

summary:
Mouse splenic dendritic cells are divided into different subsets based on their phynotype. CD8α+ and CD8α- dendritic cells play different roles against pathogens. Cross-presentation is essential for immune defense against viruses, tumors and intracellular bacteria and CD8α+ DCs are more potent in cross-presentation compared to CD8α- DCs.
We used microarrays to detail the global gene expression to analyze the underlying mechanism in CD8α+  dendritic cells cross-presentation

overall_design: Splenic CD8α+ and CD8α- dendritic cells were sorted by flow-cytometer for RNA extraction and hybridization on Affymetrix microarrays. Thirty C57BL/6J mice were sacrified for the splenic cells, splenic DCs were enriched by negtive selection, then CD8α+ and CD8α- dendritic cells were seprated based on CD11c and CD8α markers.

first: Xuetao

last: Cao


title: A YY1-dependent increase in aerobic metabolism is indispensable for intestinal organogenesis

status: Public on Aug 16 2016

first: Michael

middle: P

last: Verzi

address: 145 Bevier Rd

department: Genetics

institute: Rutgers University

summary: During late gestation, structures called villi extend into the intestinal lumen to dramatically increase the surface area of the intestinal epithelium, preparing the gut for the neonatal diet. Incomplete development of the intestine is the most common gastrointestinal complication in neonates, but the causes are unclear. We provide evidence that Yin-Yang1 (Yy1) is critical for intestinal villus development. YY1 loss in the developing endoderm had no apparent consequences until late gestation, after which the intestine differentiated poorly and exhibited severely stunted villi. Transcriptome analysis revealed that YY1 is required for mitochondrial gene expression, and ultrastructural analysis confirmed compromised mitochondrial integrity in the mutant intestine. We found increased oxidative phosphorylation gene expression at the onset of villus elongation, suggesting that aerobic respiration may function as a regulator of villus growth. Mitochondrial inhibitors blocked villus growth in a fashion similar to Yy1 loss, thus further linking oxidative phosphorylation with late-gestation intestinal development. Interestingly, we find necrotizing enterocolitis patients also exhibit decreased expression of oxidative phosphorylation genes. Our study highlights the still unappreciated role of metabolic regulation during organogenesis, and suggests it may contribute to neonatal gastrointestinal disorders.

overall_design: Mouse embryos of the same genotypes were pooled (up to 2) to obtain 2 biological replicates of YY1f/f and Yy1f/f; Shh-Cre. Epcam positive epithelium cells were enriched using magnetic selection from Small intestines of E15.5 embryos(proximal stomach to distal caecum). Cells were then dissolved in Trizol and RNA prepared by ethanol precipitation using 10ug LPA. RNA was then processed for microarray on Affymetrix Mouse 430_2 arrays according to manufacturer’s instructions.


title: The ubiquitin ligase HUWE1 regulates hematopoietic stem cell maintenance and lymphoid commitment [microarray]

status: Public on Aug 20 2016

first: Bryan

last: King

state: NY

department: Cancer Biology and Genetics

institute: Memorial Sloan Kettering Cancer Center

summary: We identified the ubiquitin ligase Huwe1 as a crucial regulator of hematopoietic stem cell (HSC) functions. We generated Huwe1 conditional knock-out mice and discovered that the loss of this ligase causes an increased proliferation and stem cell exhaustion, together with a decreased lymphoid specification in vivo. We observed that the ubiquitin ligase Huwe1 is controlling the expression of N-myc at the level of the most immature stem and progenitor hematopoietic populations, mediating the described effects.

overall_design: Hematopoietic stem cells (HSC) from the bone marrow of transgenic animals carrying a  N-myc/mCherry fusion gene were sorted according to N-myc expression (defined by mCherry) into N-myc high and low subpopulations. Each of these 2 populations was subjected to microarray gene expression profiling.

first: Francesco

middle: E

last: Boccalatte

first: Charalampos

last: Lazaris

first: Ioannis

last: Aifantis


title: Negative reciprocal regulation between Sirt1 and Per2 modulates the circadian clock and aging (microarray expression)

city: Morgantown

first: Gangqing

last: Hu

state: West Virginia

address: 64 Medical Center Drive

department: MicroBiology, Immunology, and Cell Biology

institute: West Virginia University

summary: Sirtuin 1 (SIRT1) is involved in both aging and circadian-clock regulation, yet the link between the two processes in relation to SIRT1 function is not clear. Using Sirt1-deficient mice, we found that Sirt1 and Period 2 (Per2) constitute a reciprocal negative regulation loop that plays important roles in modulating hepatic circadian rhythmicity and aging. Sirt1-deficient mice exhibited profound premature aging and enhanced acetylation of histone H4 on lysine16 (H4K16) in the promoter of Per2, the latter of which leads to its overexpression; in turn, Per2 suppresses Sirt1 transcription through binding to the Sirt1 promoter at the Clock/Bmal1 site. This negative reciprocal relationship between SIRT1 and PER2 was also observed in human hepatocytes. We further demonstrated that the absence of Sirt1 or the ectopic overexpression of Per2 in the liver resulted in a dysregulated pace of the circadian rhythm. The similar circadian rhythm was also observed in aged wild type mice. The interplay between Sirt1 and Per2 modulates aging gene expression and circadian-clock maintenance.

overall_design: To investigate hepatic SIRT1-dependent aging related genes, livers from wild type mice at 3 months (young), 12 months (middle age), and 19 months (old) of age, as well as Sirt1-deficient mice at 3 months of age were snap frozen and subject to RNA isolation and microarray analysis.

first: Wang

last: Rui-Hong

first: Zhao

last: Tingrui

first: Cui

last: Kairong

first: Hu

last: Gangqing

first: Chen

last: Qiang

last: Weiping

last: Keji

first: Deng

last: Chu-Xia


title: A transcriptomic signature of mouse liver progenitor cells

status: Public on Aug 03 2016

city: Perth

first: Adam

last: Passman

state: WA

address: 35 Stirling Highway

department: Biochemistry

country: Australia

institute: University of Western Australia

summary: A transcriptomic meta-analysis of over 400 microarrays was undertaken to compare LPC lines against datasets of; muscle and embryonic stem cell lines, embryonic and developed liver (DL), and HCC. Uploaded here, is the array data from seven of the ten LPC lines used. These seven were prepared in our laboratory. The remaining LPC arrays and arrays from other tissues/cells were obtained from the GEO.

overall_design: A total of 405 microarrays were analysed in a meta analysis. This included the 381 publically-sourced arrays (13 of which were LPC arrays) and 24 LPC arrays performed within our lab. This data was mined to obtain signature LPC pathways and novel markers. A summary of all arrays used in the analysis can be found in http://dx.doi.org/10.1155/2016/5702873

first: Jasmine

last: Low

first: Roslyn

last: London

first: Janina

last: Tirnitz-Parker

first: Atushi

last: Miyajima

first: Minoru

last: Tanaka

first: Helene

last: Strick-Marchand

first: Gretchen

last: Darlington

first: Megan

last: Finch-Edmondson

first: Scott

last: Ochsner

first: Cornelia

last: Zhu

first: James

last: Whelan

middle: A

last: Callus

first: George

middle: T

last: Yeoh


title: Genetics of the hippocampal transcriptome in mouse: a systematic survey and online neurogenomics resource

status: Public on Jul 26 2016

city: Memphis

first: Robert

middle: W.

last: Williams

state: TN

address: 71 Manassas St.

department: Department of Genetics, Genomics and Informatics

institute: University of Tennessee

summary:
The Hippocampus Consortium data set provides estimates of mRNA expression in the adult hippocampus of 99 genetically diverse strains of mice including 67 BXD recombinant inbred strains, 13 CXB recombinant inbred strains, a diverse set of common inbred strains, and two reciprocal F1 hybrids.
The hippocampus is an important and intriguing part of the forebrain that is crucial in memory formation and retrieval, and that is often affected in epilepsy, Alzheimer's disease, and schizophrenia. Unlike most other parts of the brain, the hippocampus contains a remarkable population of stems cells that continue to generate neurons and glial cells even in adult mammals (Kempermann, 2005). This genetic analysis of transcript expression in the hippocampus (dentate gyrus, CA1-CA3) is a joint effort of 14 investigators that is supported by numerous agencies described in the acknowledgments section.

overall_design: Pooled RNA samples (usually one pool of male hippocampii and one pool of female hippocampii) were prepared using standard protocols. Samples were processed using a total of 206 Affymetrix GeneChip Mouse Expression 430 2.0 short oligomer arrays (MOE430 2.0 or M430v2; see GEO platform ID GPL1261), of which 201 passed quality control and error checking. This particular data set was processed using the PDNN protocol. To simplify comparisons among transforms, PDNN values of each array were adjusted to an average of 8 units and a standard deviation of 2 units.

middle: W

first: David

middle: C

last: Airey

first: Dan

last: Goldowitz

first: Rupert

last: Overall

first: Gerd

last: Kempermann

first: Jeremy

last: Peirce

first: Lu

last: Lu

first: Fred

last: Gage

first: Shirlean

last: Goodwin

first: August

middle: B

last: Smit

first: Glenn

middle: D

last: Rosen

first: Leonard

last: Schalkwyk

first: Thomas

middle: R

last: Sutter

first: Richard

middle: S

last: Nowakowski

first: Stephen

last: Whatley


title: In vivo Gene Expression Profiling of RPE/choroid Post-Intravitreal Injections of Dexamethasone and Triamcinolone at Clinically Relevant Time Points for Patient Care

city: Davis

first: Zeljka

last: Smit-McBride

state: CA

address: One Shields Ave, Tupper Hall #2403

department: Ophthalmology & Vision Science

institute: University of California, Davis Eye Center

summary: PURPOSE   To identify retinal pigment epithelial (RPE)/choroid genes and their relevant expression pathways affected by intravitreal injections of dexamethasone and triamcinolone acetonide in mice at clinically relevant time points for patient care.   METHODS   Differential gene expression of over 34,000 well-characterized mouse genes, in the RPE/choroid of 6 week old C57BL/6J mice were analyzed after intravitreal steroid injections at 1 week and 1 month post injection, using Affymetrix Mouse Genome 430 2.0 microarrays.  The data were analyzed using GeneSpringGX12.5 and Ingenuity Pathway Analysis (IPA) microarray analysis software for biologically relevant changes.    RESULTS   Both triamcinolone and dexamethasone caused differential activation of genes involved in ‘Circadian Rhythm Signaling’ pathway at both time points tested.  Triamcinolone (TAA) uniquely induced significant changes in gene expression in ‘Calcium Signaling’ (1 week) and ‘Glutamate Signaling’ pathways (1month).  In contrast, Dexamethasone (Dex) affected the ‘GABA Receptor Signaling’ (1 week) and ‘Serotonin Receptor Signaling’ (1month) pathways.    CONCLUSIONS  Understanding how intraocular steroids affect the gene expression of RPE/choroid is clinically relevant.  This in vivo study has elucidated several genes and pathways that are potentially altering the circadian rhythms and several other neurotransmitter pathways in RPE/choroid cells during intravitreal steroid injections, which likely has consequences in the dysregulation of RPE function and neurodegeneration of the retina.

overall_design: Total of 18 RPE/choroid samples were analysed. There were two time points, day7 and day30. Each time point had three groups: BSS control, DEX treatment and TAA treatment. Each group had three biological replicas.


title: The essential role of PBX1, a stem cell reprogramming factor, in ovarian cancer chemoresistance

status: Public on Jul 25 2016

city: baltimore

first: Jin

last: Jung

state: MD

address: 1550 orleans street, CRB2, Rm 376

department: OB/GYN

institute: Johns Hopkins Medical Institutes

summary: Elucidating the pathogenesis of chemoresistance is fundamental for developing more effective interventions that will improve the clinical outcome of neoplastic diseases such as ovarian cancer. Here, we report the upregulation of PBX1, a stem cell reprogramming factor, in recurrent ovarian carcinomas. Moreover, high levels of PBX1 expression are correlated with a shorter survival rate among post-chemotherapy ovarian cancer patients. Ectopic expression of PBX1 promotes cancer stem cell-like phenotypes, including increased side population and ALDH activity, enhanced tumorigenicity at a low cell density, and increased resistance to platinum-based therapy. Silencing PBX1 in platinum-resistant cell lines that overexpress PBX1 sensitizes cells to platinum treatment and reduces their “stemness”. Analysis of previously reported genome-wide chromatin immunoprecipitation data shows that PBX1 binds directly to promoters of genes involved in stem cell maintenance and tissue injury response. We confirmed direct regulation of STAT3 by PBX1, and demonstrated that the PBX1 binding motif located on the STAT3 promoter participates in positive transcriptional regulation of STAT3. Furthermore, a STAT3/JAK2 inhibitor potently sensitizes platinum-resistant cells to carboplatin and suppresses their growth in vivo. These findings establish PBX1 as an upstream regulator of key pathways in stem cell and tissue damage response and highlight the potential of targeting the PBX1/STAT3 axis to overcome chemoresistance in human cancers.

overall_design: Determine gene expression changes after knockdown of PBX1 protein in an ovarian cancer cell line (OVCAR3)

first: Michelle

last: Thiaville

first: Jin-Gyoung

first: Tian-Li

last: Wang


title: c-Jun protein expression in vivo induces systemic fibrosis in mice

city: stanford

first: Gerlinde

last: Wernig

address: 265 Campus Drive

department: Pathology

institute: Stanford

summary: Time course analysis of c-Jun expression at 24h resulted in upregulation of a number of well-known fibrogenesis-associated factors.

overall_design: We compared the global gene expression pattern of mouse whole bone marrow after c-Jun induction in vivo at 24h with no induction and applied to standard Affymetrix mouse arrays.

first: Jonathan

last: Jesneck


status: Public on Jul 21 2016

city: Columbus

first: Sashwati

last: Roy

state: OH

department: Surgery

institute: Ohio State University

summary:
Gene Expression in d5 wound-edge tissues of MFG-E8 WT and MFG-E8 KO mice
Affymetrix GeneChip® Mouse Genome 430 array  was used to study the gene expression in d5 wound-edge tissues of MFG-E8 WT and MFG-E8 KO mice

first: Roy

last: Sashwati


title: Expression data from ileum of mice suffered from subchronic and mild social defeat stress

city: Tsukuba

first: Chise

last: Suzuki

state: Ibaraki

address: 2 Ikenodai

department: Animal Products Res. Division

institute: NARO Institute of Livestock and Grassland Science

summary:
This study aimed to investigate the effects of depression on transcriptome in ileum using a subchronic and mild social defeat stress (sCSDS) model. In addition to exhibiting social deficit and hyperphagia-like behavior, the sCSDS mice keep much more water in their body than control mice. In order to investigate the effect of social defeat stress on not only central nervous system but also function of gastrointestinal tract, the gene expression in ileum of stressed mice was compared with control mice.
We used microarrays to detail the gene expression after 10 days of social defeat stress and identified distinct classes of down-regulated genes during this process.

overall_design: The duration of physical contacts was set at 5 min after the first attack bite at Day 1, and then was reduced 0.5 min per day from Day 2 to Day 10.

first: Ayako

last: Aoki-Yoshida

first: Reiji

last: Aoki

first: Tatsuhiko

last: Goto

first: Atsushi

last: Toyoda


title: Sphingosine-1-phosphate Phosphatase 2 Regulates Pancreatic Islet β-cell Endoplasmic Reticulum Stress and Proliferation

city: Bethesda

first: WeiPing

last: Chen

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

department: GCL

institute: NIDDK/NIH

summary: Sphingosine-1-phosphate (S1P) is a sphingolipid metabolite that regulates basic cell functions through metabolic and signaling pathways. Intracellular metabolism of S1P is controlled, in part, by two homologous S1P phosphatases, 1 and 2, which are encoded by Sgpp1 and Sgpp2, respectively. S1P phosphatase activity is needed for efficient recycling of sphingosine into the sphingolipid synthesis pathway. S1P phosphatase 1 is important for skin homeostasis, but little is known about the functional role of S1P phosphatase 2. To identify the functions of S1P phosphatase 2 in vivo, we studied mice with the Sgpp2 gene deleted. In contrast to Sgpp1-/- mice, Sgpp2-/- mice had normal skin and were viable into adulthood. Unexpectedly, WT mice expressed Sgpp2 mRNA at high levels in pancreatic islets when compared with other tissues. Sgpp2-/- mice had normal blood insulin levels and pancreatic islet size; however, Sgpp2-/- mice treated with a high-fat diet (HFD) had significantly lower blood insulin levels and smaller pancreatic islets compared with WT mice. The smaller islets in the HFD-treated Sgpp2-/- mice had a significantly lower adaptive β-cell proliferation rate in response to the diet compared with HFD-treated WT mice. Importantly, β-cells from Sgpp2-/- mice fed a normal diet showed significantly increased expression of proteins characteristic of the endoplasmic reticulum (ER) stress response compared with β-cells from WT mice. Our results suggest that Sgpp2 deletion causes β-cell ER stress, which is a known cause of β-cell dysfunction, and reveal a novel juncture in the sphingolipid recycling pathway that could impact the development of diabetes.

overall_design: Three replications of Mouse (WT vs KO) that were treated with with Normal and HFD foods.

first: Yoshimitsu

last: Taguchi

first: Maria

middle: L

last: Allende

first: Hiroki

last: Mizukami

first: Emily

middle: K

last: Cook

first: Oksana

last: Gavrilova

first: Galina

last: Tuymetova

first: Benjamin

last: Clarke

first: Weiping

first: Ana

last: Olivera

last: Proia


title: Gfi1 as a new predictive and therapeutical target of MDS/AML

status: Public on Jul 31 2016

city: Essen

first: Cyrus

last: Khandanpour

address: Hufelandstr. 55

department: Hematology

country: Germany

institute: University Hospital Essen

summary:
MDS is characterized by a disturbed function of the myeloid lineage of the hematopoietic system that may transform to AML, a malignant disease of the myeloid compartment. Epigenetic and genetic aberrations contribute to the initiation and progression of MDS/AML. GFI1 is a transcriptional repressor, which regulates expression of its target genes by, among other approaches, recruiting HDACs to its target genes to remove histone 3 lysine 9 (H3K9) acetylation, a marker for active gene expression. Low levels of GFI1 expression and deletion of one GFI1 allele contribute to MDS/AML development in human patients and are associated with a specific gene expression signature and inferior prognosis. To explore the mechanism behind this, we used a mouse strain, which expresses GFI1 only at 5-10% of the normal level (GFI1-Knock-down (KD)). Knock-down of GFI1 or loss of one murine Gfi1 allele reduced latency and increased incidence of AML in different murine models of human MDS/AML development. On the epigenetic level, KD of Gfi1 lead to increased amount of H3K9 acetylation, resulting in increased expression of genes involved in AML development. On a translational level both murine as well as human AML cells with low expression of GFI1 are resistant to standard epigenetic therapy. We show that treatment with histone acetyltransferase inhibitors might be a novel treatment approach for low Gfi1-expressing blast cells. GFI1 has a dose dependent role in myeloid malignancies and is a biomarker for therapeutic intervention.
We used microarrays to detail the global programme of gene expression in bone marrow cells of Nup98HoxD13 leucemic mice and identified distinct classes of up-regulated genes during this process.

overall_design: Bone marrow cells of leukemic mice (from KI & KD Nup98HoxD13 mice) were collected for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain homogeneous populations of leukemic cell population, so we took samples of mice which had the same age.

first: J

last: Hoenes

first: C


title: Gene expression analysis in cortex of CRTC1 deficient mice and WT littermates

status: Public on Jul 18 2016

city: Lausanne

first: Tamara

last: Seredenin

address: AI2135 Station 15 EPFL

country: Switzerland

institute: EPFL

summary:
To identify gene expression changes associated with Crtc1 deficiency, we performed genome-wide transcriptome profile analyses by using mouse cDNA microarrays in the cortex of Crtc1‒/‒ and WT female mice
BACKGROUND: Recent studies involve the arginine-decarboxylation product agmatine in mood regulation. Agmatine has antidepressant properties in rodent models of depression, and agmatinase (Agmat), the agmatine-degrading enzyme, is upregulated in the brain of mood disorders patients. We showed that mice lacking CREB-regulated transcription coactivator 1 (CRTC1) associate neurobehavioral and molecular depressive-like endophenotypes, as well as blunted responses to classical antidepressants.  METHODS: The molecular basis of the behavioral phenotype of Crtc1‒/‒ mice was further examined using microarray analysis. We characterized Agmat expression in the prefrontal cortex (PFC) and hippocampus (HIP) by quantitative polymerase chain reaction (qPCR), Western blot (WB) analysis, and confocal immunofluorescence microscopy. The antidepressant effect of agmatine was assessed by the forced swim test (FST). Brain-derived neurotrophic factor (BDNF) levels and eukaryotic elongation factor 2 (eEF2) phosphorylation were measured by WB.  RESULTS: Microarray, qPCR and WB analyses revealed an upregulation of Agmat in Crtc1‒/‒ PFC and HIP, where immunofluorescence microscopy showed more Agmat-expressing cells, notably parvalbumin- and somatostatin-interneurons. Acute agmatine treatment efficiently improved depressive-like behavior of Crtc1‒/‒ mice in the FST, suggesting that exogenous agmatine has a rapid antidepressant effect through the compensation of agmatine deficit induced by upregulated Agmat. In WT mice, agmatine rapidly increased BDNF levels and eEF2 dephosphorylation, indicating that it might be a fast–acting antidepressant with NMDA receptor antagonist properties.  CONCLUSIONS: Collectively, these findings support the involvement of the agmatinergic system in the depressive-like phenotype of Crtc1‒/‒ mice, and allow a better understanding of the agmatinergic system and its putative role in major depression.

overall_design: RNA from cortex of 5 WT and 5 KO mice was used

last: Seredenina

first: Lionel

last: Breuillaud

first: Ruth

last: Luthi-Carter

first: Jean-René

last: Cardinaux


title: Rictor Plays a Pivotal Role in Maintaining Quiescence as well as Stemness of Leukemia Stem Cells in MLL-Driven Leukemia

status: Public on Jul 19 2016

city: Wuhan

first: Yang

last: Yang

address: #1095,Jiefang Avenae

institute: Tongji Hospital

summary:
Little is known about the roles of Rictor/mTORC2 in the leukemogenesis of AML. Here, we demonstrated that Rictor is essential for the maintenance of MLL-driven leukemia by preventing LSCs from exhaustion. Rictor depletion led to a reactive activation of mTORC1 signaling by facilitating the assembly of mTORC1. Hyperactivated mTORC1 signaling in turn drove LSCs into cycling, compromised the quiescence of LSCs and eventually exhausted their capacity to generate leukemia.
At the same time, loss of Rictor had led to a reactive activation of FoxO3a in leukemia cells, which acts as negative feedback to restrain greater over-reactivation of mTORC1 activity and paradoxically protects leukemia cells from exhaustion. Simultaneous depletion of Rictor and FoxO3a enabled rapid exhaustion of MLL LSCs and a quick eradication of MLL leukemia. As such, our present findings highlighted a pivotal regulatory axis of Rictor-FoxO3a in maintaining quiescence and the stemness of LSCs.

overall_design: To understand the critical molecular events caused by Rictor loss in MLL-AF9-driven leukemia,the K+G– mice BM cells  were sorted from the 1st BMT of RictorΔ/Δ(MA9_R1,MA9_R2,MA9_R3) or control(MA9_C1,MA9_C2,MA9_C3), and subjected to microarray analysis on Affymetrix microarrays.Furthermore, the MLL-NRIP3-driven mice model was chosen for further examination.The K+G– mice BM cells  were sorted from the 1st BMT of RictorΔ/Δ(MN3_R1,MN3_R2,MN3_R3) or control(MN3_C1,MN3_C2,MN3_C3), and subjected to microarray analysis on Affymetrix microarrays.

first: Yong

last: Fang

first: Jianfeng

last: Zhou


title: Microarray analysis of striatal tissue of wild type and Ezh1/Ezh2 dKO mice at 6 weeks, 3 months, and 6 months

status: Public on Jul 29 2016

city: New York

first: Josefa

last: Sullivan

address: 1425 Madison Ave

department: Neuroscience

institute: Icahn School of Medicine at Mount Sinai

summary: Normal brain function critically depends on the interaction between highly specialized neurons that operate within anatomically and functionally distinct brain regions. The fidelity of neuronal specification is contingent upon the robustness of the transcriptional program that supports the neuron type-specific patterns of gene expression. Changes in neuron type-specific gene expression are commonly associated with neurodegenerative disorders including Huntington’s and Alzheimer’s disease. The neuronal specification is driven by gene expression programs that are established during early stages of neuronal development and remain in place in the adult brain. Here we show that the Polycomb repressive complex 2 (PRC2), which supports neuron specification during early differentiation, contributes to the suppression of the transcription program that can be detrimental for the adult neuron function. We show that PRC2 deficiency in adult striatal neurons and in cerebellar Purkinje cells impairs the maintenance of neuron-type specific gene expression. The deficiency in PRC2 has a direct impact on a selected group of genes that is dominated by self-regulating transcription factors normally suppressed in these neurons. The age-dependent progressive transcriptional changes in PRC2-deficient neurons are associated with impaired neuronal function and survival and lead to the development of fatal neurodegenerative disorders in mice.

overall_design: There are 23 total samples. There are three ages, 6 weeks, 3 months and 6 months. There are at least three biological replicates per group. Control samples are age- and sex-matched littermates.

first: Melanie

last: von Schimmelmann

first: Philip

last: Feinberg

first: Stacy

last: Ku

last: Badimon

first: Mary

last: Duff

first: Zichen

last: Wang

first: Alexander

last: Lachmann

first: Scott

last: Dewell

first: Avi

last: Ma'ayan

first: Ming-Hu

last: Han

last: Tarakhovsky

first: Anne

last: Schaefer


title: Expression data during vascular endothelial cells differentiation from mouse embryonic stem cells

city: Tokyo

first: Yasuharu

last: Kanki

address: 4-6-1 Komaba, Meguro-ku

institute: The University of Tokyo

summary: Although differentiation of mice embryonic stem cells into vascular endothelial cells (ECs) gives a model for investigating molecular mechanisms of vascular development in vivo, temporal dynamics of gene expressions and chromatin modifications have not been studied until now. Here, we interrogated transcriptome and two histone modifications, H3K4me3 and H3K27me3, with a genome-wide scale during ECs differentiation and elucidated epigenetic switch peculiar to ECs. We find Gata2, Fli1, Sox7, and Sox18 are master regulators from genetic and epigenetic data, these genes were induced after Etv2 activation. These genes have specific histone modification pattern which is repressed by H3K27me3 modification at Flk-sorted mesoderm and changed to the bivalent (H3K4me3 and H3K27me3 both positive) state rapidly after vascular endothelial cells growth factor (VEGF) stimuli. Using a previously reported ECs differentiation model, we demonstrate that four transcription factors are critical for ECs specific gene expressions and efficient differentiation. Moreover, from knockdown experiments using si-RNA, we discovered these factors inhibited not only TGFβ signaling pathway, that is endothelial mesenchymal transition pathway, but also other near lineage commitment, including blood cells, skeletal muscle cells, vascular smooth muscle cells, and cardiomyocytes. We further identify each factor specific target genes during ECs differentiation by microarray, including both activating and repressing genes. Together, our findings from a detailed epigenetic approach provide a basic understanding temporal regulated chromatin signatures and resulting gene expression profile during ECs commitment, which is applicable to other models of differentiation and production of mature and long lasting ECs for regenerative medicine.

overall_design: Total 17 samples were derived from [1] ES cells, Flk-sorted mesoderm cells, and in the absense or presence of VEGF (6, 12, 24, and 48h) to determine VEGF activated genes during endothelial cells differentiation, [2] control si-RNA, si-Gata2, si-Fli1, si-Sox7, or si-Sox18 transfected cells under VEGF stimuli, [3] control si-RNA or si-Mix (si-Gata2, si-Fli1, si-Sox7, and si-Sox18) transfected cells under VEGF stimuli for the identification of each transcription factor dependent genes during endothelial cells differentiation.

first: Takashi

last: Minami


title: Expression microarray analysis of RHOXF1 and RHOXF2 transfected HEK293 cells

status: Public on Jul 16 2016

city: Münster

first: Jennifer

last: Borgmann

address: Albert-Schweitzer Campus 1, Building D11

department: Centre of Reproductive Medicine and Andrology

institute: University Hospital Muenster

summary: The X-linked reproductive homeobox (RHOX) gene cluster encodes transcription factors displaying preferential expression in reproductive tissues. They have important roles in human male fertility based on phenotypic defects of Rhox-mutant mice and the finding that aberrant RHOX promoter methylation is strongly associated with abnormal human sperm parameters. The aim of this study was to analyze the molecular mechanism of RHOX action in humans. Using genome-wide analysis, we investigated the identity of genes regulated by the known human RHOX transcription factors: RHOXF1 and RHOXF2/2B. HEK293 cells were transiently transfected with either RHOX expression (RHOXF1; RHOXF2) or an empty control vector. Afterwards, differently expressed genes were identified by microarray analysis after 24h and 48h of transfection. Thereby we could identify genes that are differently regulated in response to RHOX overexpression.

overall_design: Total RNA was isolated from RHOX (RHOXF1; RHOXF2) and control transfected HEK293 cells after 24h and 48h of transfection. Affymetrix GeneChip Human Exon 1.0 ST arrays were used to evaluate changes in mRNA expression in RHOX transfected samples compared to control transfected samples (analyzed in biological triplicates). Data were processed and analyzed using Affymetrix Gene Expression Console and Affymetrix transcriptome analysis console.

first: Sandra

last: Laurentino

first: Jörg

last: Gromoll


title: Nerve-derived Schwann cell precursors, acting in a paracrine fashion, are essential for mammalian digit tip regeneration

status: Public on Jul 12 2016

city: Toronto

first: Freda

last: Miller

state: ON

address: 686 Bay St

country: Canada

institute: Hospital for Sick Children

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

sample_organism:
Mus musculus
Rattus norvegicus

platform_organism:
Mus musculus
Rattus norvegicus

overall_design: Refer to individual Series


title: Nerve-derived Schwann cell precursors, acting in a paracrine fashion, are essential for mammalian digit tip regeneration [RAT]

summary: Multi-tissue regenerative capacity is lost in adult mammals with the exception of the distal digit, which regenerates via largely-uncharacterized mechanisms.  Here, we demonstrate that following adult mouse distal digit removal, nerve-associated Schwann cell precursors (N-SCPs) dedifferentiate and secrete growth factors that promote expansion of the blastema and digit regeneration.  Specifically, when N-SCPs were dysregulated or ablated, mesenchymal precursor proliferation in the blastema was decreased, nail and bone regeneration were impaired, and regeneration could be rescued by transplantation of exogenous N-SCPs.  We show that N-SCPs secreted factors that promoted self-renewal of mesenchymal precursors, and we used transcriptomic and proteomic analysis to define candidate factors. Two of these, oncostatin M (OSM) and PDGF-AA, were made by N-SCPs in the regenerating digit, and rescued the deficits in regeneration caused by loss of N-SCPs due to denervation.  Since nerves innervate every peripheral tissue, these results have broad implications for mammalian tissue repair and regeneration.

overall_design: We obtained three independent isolates of back skin SKPs and sciatic nerve NSCPs from newborn Sprague-Dawley rat pups

first: Adam

last: Johnston

last: Yuzwa

first: Matthew

middle: J

last: Carr

first: Neemat

last: Mahmud

first: Mekayla

last: Storer

last: Krause

first: Karen

last: Jones

first: Smitha

last: Paul

first: David

last: Kaplan


title: Expression data from whole lateral ventricle choroid plexus tissue of young (two months old) and aged (eighteen months old) CD1 male mice.

status: Public on Jul 20 2016

city: Ann Arbor

first: Dogukan

last: Mizrak

state: MI

address: NCRC Building 26, 263S

department: Cardiac Surgery

institute: University of Michigan

summary: We used microarrays to reveal the global expression profiles of young and old whole lateral ventricle choroid plexus tissue.

overall_design: RNA was isolated from whole lateral ventricle choroid plexus tissue followed by RNA amplification and hybridization on Affymetrix microarrays. Each sample contains both lateral ventricle choroid plexi from one male CD1 mouse. A total of six samples (three biological replicates from 2 different ages) were analyzed.

first: Violeta

last: Silva-Vargas

first: Angel

last: Maldonado-Soto

first: Paolo

last: Codega

first: Fiona

last: Doetsch


title: Microarray analysis of Mef2c deficient and control bone marrow pre-B and pro-B cells

city: Los Angeles

first: Wenyuan

last: Wang

state: cA

address: 651 Charles E Young Drive

institute: UCLA


title: Microarray analysis of Mef2c deficient and control bone marrow pro-B cells

summary:
Gene expression of mice bone marrow pro-B cells from both control and Vav-Cre Mef2cfl/fl mice (9 months old)
We used these microarrays to identify the function of MEF2C in BM B lymphoid progenitors

overall_design: Gene expression analysis of freshly FACS sorted BM B cell progenitors using Affymetrix microarray analysis [pro-B cells]

first: Amélie

last: Montel-Hagen

first: Hanna

last: Mikkola


title: miRNA expression profile of PBMCs in healthy subjects after extra virgin olive oil (EVOO) intake - Part 2 (Controls)

city: Bari

first: Antonio

last: Moschetta

address: Via Orazio Flacco, 65

country: Italy

institute: IRCCS Ospedale Oncologico di Bari

summary: miRNA expression profiles of PBMCs in healthy subjects following extra virgin olive oil intake. The aim of the present study was to investigate the whole-genome gene and miRNA profiles of PBMCs after EVOO intake. Results provide the information of changes in PBMPs transcriptome following EVOO intake.

overall_design: RNA obtained from PBMCs of the same patients before and after extra virgin olive oil intake (paired samples). Comparisons: T0 vs. T1 (paired samples) - Controls

first: Simona

last: D'Amore

first: Andria

last: D'Orazio

first: Giusi

last: Graziano

first: Michele

last: Vacca


title: Microarray analysis of Mef2c deficient and control bone marrow pre-B cells

summary:
Gene expression of mice bone marrow pre-B cells from both control and Vav-Cre Mef2cfl/fl mice (9 months old)
We used these microarrays to identify the function of MEF2C in BM B lymphoid progenitors

overall_design: Gene expression analysis of freshly FACS sorted BM B cell progenitors using Affymetrix microarray analysis [pre-B cells]


title: Patterns of gene expression among murine models of hemorrhagic shock trauma and sepsis

status: Public on Jul 10 2016

city: Gainesville

first: M Cecilia

last: Lopez

state: FL

address: 1376 Mowry Road

department: Molecular Genetics and Microbiology

institute: University of Florida

summary: The PT , PT + PP, and CLP murine models have unique transcriptomic respones 2 hrs, 1 and 3 days after injury

overall_design: We used mouse microarrays to detail the molecular profile of the events that occur following injury in mice models

first: Benjamin

last: Szpila

first: Dina

last: Nacionales

first: M

first: Lori

middle: F

last: Gentile

first: Brittany

last: Mathias

first: Erin

last: Vanzant

first: Ricardo

last: Ungaro

last: Holden

first: Martin

last: Rosenthal

first: Frederick

last: Moore

first: Henry

middle: V

last: Baker

first: Lyle

last: Moldawer

first: Philip

last: Efron


title: Microarray analysis reveals differential effects of conjugated linoleic acid isomers in ritonavir-treated 3T3-L1 adipocytes

status: Public on Jul 07 2016

city: London

first: Matthew

last: Arno

state: LONDON

address: 150 Stamford Street

department: Genomics Centre

country: United Kingdom

institute: King's College London

summary:
Objective: To quantify changes in adipogenic gene expression in the presence of ritonavir (RTV) or tenofovir (TDF), and determine whether conjugated linoleic acid (CLA) isomers (cis9,trans11 or trans10,cis12) can mitigate detrimental effects of antiretoviral drugs.
Methods: Affymetrix Mouse Genome 430 2.0 microarray was used to investigate gene expression in 3T3-L1 adipocytes treated with (1) RTV, TDF or ethanol control, or (2) ritonavir +c9,t11-CLA, ritonavir+t10,c12-CLA or ritonavir+DMSO control. RT-PCR validation of Pparg, Adipoq and Retn was carried out. ELISA and DNA binding ELISA were used to investigate secreted proteins and Pparg binding to its gene response element. Oil Red O staining was used to investigate triglyceride accumulation.
Results: No effect was observed for TDF. Expression of 389 genes was altered more than 5-fold in the presence of RTV. Down-regulated genes included Pparg, Adipoq, Retn, Cfd and Cidec. Pparg and Adipoq down-regulation were confirmed by RT-PCR. PPAR-γ binding to its gene response element, adiponectin protein secretion and triglyceride accumulation were decreased by RTV. t10,c12-CLA in the presence of RTV decreased the expression of Ppargand Adipoq in microarray and RT-PCR. c9,t11-CLA increased PPAR-γ binding to its gene response element. Both isomers increased triglyceride storage in the presence of RTV.
Conclusion: Ritonavir altered genes involved in adipocyte differentiation, lipid accumulation and glucose metabolism. Down-regulation of Pparg may be mediated by changes in Cepba and regulatory genes Pparg1c and Nr1h3.

overall_design: 3T3-L1 adipocytes were treated with ritonavir (20μM; n=4), tenofovir (1μM; n=4) or vehicle control (ethanol 0.1%; n=4) for 5 days and in a second experiment with ritonavir (20 µM) +c9,t11-CLA (100μM; n=4), ritonavir (20 µM) +t10,c12-CLA (100μM; n=4) or ritonavir+fatty acid vehicle control (DMSO 0.1%; n=4) for 5 days.

first: Cathriona

last: Loonam

first: Sandra

last: O'Dell

first: Paul

last: Sharp

first: Anne

last: Mullen


title: Interferon-alpha signaling promotes AGM HSC maturation

status: Public on Jul 11 2016

city: Boston

first: Peter

middle: Geon

last: Kim

state: MA

address: 360 Longwood Ave, Lc8202

department: Hematology/Oncology

institute: Dana Farber Cancer Institute

summary:
Interferon-alpha promotes engraftment of mid-gestation hematopoietic stem cells by promoting competitiveness and restore the hematopoietic defect of Arid3a knockout embryos
We used microarray to response of AGM HSCs (VE+CD45+) to IFNa (0.5ng/ml) treatment for 4 hours

overall_design: Isolated VE+CD45+ cells from E11.5 AGM were treated with IFNa (0.5ng/ml) in 10% FBS/IMDM for 4 horus before RNA isolation. RNA was NuGen amplified.

middle: G

first: George

middle: Q

last: Daley


title: Regulatory T cell modulation by CBP/EP300 bromodomain inhibition [array]

status: Public on Jul 06 2016

city: Cambridge

first: Barbara

middle: M

last: Bryant

address: 215 First Street

institute: Constellation Pharmaceuticals

summary: Genome-wide gene expression changes in response to CBP inhibitor treatment in Treg cells using microarray.

overall_design: Expression profiling by microarray of Treg cells treated with DMSO or CBP inhibitor, and Th0 cells

first: Srimoyee

last: Ghosh

first: Jose

last: Lora

first: Robert

last: Sims

first: Melissa

last: Chin

first: Hon-Ren

last: Huang

first: Andres

last: Salmeron

first: Pranal

last: Dakle

first: Deanna

last: Mele

first: Charlie

last: Hatton


title: Inhibition of beta-catenin signalling in dermal fibroblasts enhances hair follicle regeneration during wound healing

city: San Francisco

first: Angela

last: Oliveira Pisco

address: 499 Illinois St

department: Data Science

institute: Chan Zuckerberg Biohub

summary: We performed gene expression profiling of P1 and P5 back and tail dermis to uncover potential explanations for the differences in HF formation at different ages and in different body sites.

overall_design: To generate back and tail dermis microarray from P1 mouse (C57Bl6/CBA F1), tail skin was incubated in 5mM EDTA/PBS solution at 37°C, 1h, whereas back skin was incubated in dispase-trypsin solution at 37°C, 1h. Tail and back skin dermis were separated from the epidermis with forceps, washed once in PBS and digested as described above. Single-cell suspensions were washed 3x in PBS, before cells were lysed in Trizol (Invitrogen) and RNA was purified using Qiagen RNeasy columns. RNA was extracted from triplicate mice. cDNA was amplified from purified RNA and hybridized to Affymetrix MG430.2A arrays by the Cancer Research UK Patterson Institute Affymetrix Genechip Microarray Service.  Array images were produced by the Affymetrix PICR 3000 scanner and analysed as Cell files using Genespring-13X (Agilent Technologies). RMA normalization was used and the bottom twentieth-percentile of genes (i.e., the 20% of genes with the lowest expression levels) were excluded from subsequent analysis.

first: Celine

last: Gomez

middle: O

last: Pisco

first: Fiona

last: Watt


title: Mesenchymal stromal cells isolated from bronchoalveolar lavage and digest parenchymal lung tissue

status: Public on Jul 04 2016

city: St. Lucia

first: Othmar

last: Korn

state: Queensland

address: University of Queensland

institute: Australian Institute for Bioengineering and Nanotechnology

summary: Stromal support is critical to the achievement of lung homeostasis and the maintenance of an effective epithelial barrier, and yet previous studies have found a positive association between the number of mesenchymal stromal cell populations (MSCs) isolated from the alveolar space and human diseases associated with epithelial dysfunctional. We hypothesised that alveolar MSCs (A-MSCs) represent a dysfunctional population which would be distinct from lung tissue MSCs (LT-MSCs) and which would not be recoverable from healthy humans. In this study, we comprehensively interrogated the phenotype and transcriptome of human A-MSCs and LT-MSCs. We found that MSCs were rarely recoverable from the alveolar space in healthy humans, but were readily isolated from lung transplant recipients, where they expressed a CD90Hi, CD73Hi, CD45Neg, CD105Lo immunophenotype and were bipotent, lacking adipogenic potential. In contrast, MSCs were readily recoverable from healthy lung tissue and were CD90Hi or Lo, CD73Hi, CD45Neg, CD105Int and had full tri-lineage potential. Transcriptome profiling of the two populations confirmed their status as MSCs and revealed a high degree of similarity between each other and the archetypal bone-marrow MSC. 105 genes were differentially expressed, with genes involved in fibroblast activation, extracellular matrix deposition and tissue remodelling being up-regulated in A-MSCs. Finally, we found the fibroblast markers collagen 1 and α-smooth muscle actin was increased in A-MSCs. Our data suggest that in healthy humans, lung MSCs reside within the tissue, but in disease can differentiate to acquire a profibrotic phenotype and so move out of their niche into the alveolar space.

overall_design: Total RNA obtained from in vitro expanded MSCs (p2-4)

first: Kenneth

middle: A

last: Sinclair

first: Stephanie

middle: T

last: Yerkovich

first: Tyrone

last: Chen

first: Jonathan

last: McQualter

last: Hopkins

first: Christine

last: Wells

first: Daniel

last: Chambers


title: Gene expression data from murine myeloid leukemia genomes induced by Sleeping Beauty transposon mutagenesis

city: Tampa

first: Michael

middle: B.

last: Mann

state: Florida

address: 12902 Magnolia Drive

department: Molecular Oncology

institute: H. Lee Moffitt Cancer Center and Research Institute

summary: Transcriptome analysis of mRNA samples from a cohort of mice with histopathologically diagnosed Undifferentiated Myeloid Leukemia.

overall_design: Tissues from flash frozen leukemic spleen was collected at necropsy from 47 mice with myeloid leukemia (22 males, 25 females) using the Affymetrix Mouse Genome 430 2.0 Array platform (GPL126). Array data was processed using the RMA algorithm as implemented in the affy package for R. No techinical replicates were performed.

first: Karen

last: Black

first: Leslie

last: McNoe

first: Luxmanan

last: Selvanesan

first: Jerrold

last: Ward

first: Nancy

last: Jenkins

first: Neal

last: Copeland


title: Mouse myoblasts grown on Fibronectin or Collagen I for 72 hours

first: Jerome

last: Feige

address: EPFL Innovation Park, Building H

department: Musculo-Skeletal Health

institute: Nestle Institute Of Health Sciences

summary: The goal of this study was to investigate the transcriptional regulation in cells grown on Fibronectin when compared to Collagen I

overall_design: 3 samples per condition

first: Florian

last: Bentzinger

first: Eugenia

last: Migliavacca

first: Sylviane

last: Metairon

first: Frederic

last: Raymond

middle: N


title: Olfactomedin 4 deficiency promotes prostate neoplastic progression and is associated with upregulation of the hedgehog-signaling pathway

city: Bethesda

first: WeiPing

last: Chen

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

institute: NIDDK/NIH

summary: Loss of olfactomedin 4 (OLFM4) gene expression is associated with the progression of human prostate cancer, but its role and the molecular mechanisms involved in this process have not been completely understood. In this study, we found that Olfm4-knockout mice developed prostatic intraepithelial neoplasia and prostatic adenocarcinoma. Importantly, we found that the hedgehog-signaling pathway was significantly upregulated in the Olfm4-knockout mouse model. We also found that restoration of OLFM4 in human prostate-cancer cells that lack OLFM4 expression significantly downregulated hedgehog signaling-pathway component expression. Furthermore, we demonstrated that the OLFM4 protein interacts with sonic hedgehog protein, as well as significantly inhibits GLI-reporter activity. Bioinformatic and immunohistochemistry analyses revealed that decreased OLFM4 and increased SHH expression was significantly associated with advanced human prostate cancer. Thus, olfactomedin 4 appears to play a critical role in regulating progression of prostate cancer, and has potential as a new biomarker for prostate cancer.

overall_design:
Purpose: To explore the mechanisms underlying increased tumorigenesis of Olfm4-deficient murine prostate.
Experiment design: Comparison of gene expression between Olfm4-knockout and wild-type mice at 3 months of age in the prostate tissue.
Experimental procedures: Total RNA was purified from whole prostate tissue of Olfm4 (+/+) and Olfm4 (-/-) mice at 3 months of age using the RNeasy Plus Mini Kit (Qiagen). Microarray analyses were performed by the NIDDK Core Facility at the National Institutes of Health using Affymetrix Mouse Genome 430 2.0 Array GeneChips (Affymetrix; Santa Clara, CA).  Biological replications were used for the Olfm4 (+/+) or Olfm4 (-/-) prostate RNA extracted from five individual mice. The microarray signals were analyzed using the Affymetrix RMA algorithm. The analysis of variance results, False Discovery Rate (FDR) reports, and heatmaps were generated using Partek Genomic of tware 6.5 (Partek; St. Charles, MO). Pathway analyses were performed using MetaCore webaccess software (http://www.genego.com/).

first: Hongzhen

last: Li

first: Wenli

last: Liu

first: Chu-Xia

last: Deng

first: Jianqiong

last: Zhu

first: Weiping

first: Griffin

middle: P

last: Rodgers


title: Control of the inflammatory macrophage transcriptional signature by miR-155

status: Public on Jul 15 2016

city: Columbus

first: Mireia

last: Guerau

address: 453 W 10th Ave

department: HRS-Medical Laboratory Science

institute: The Ohio State University

summary: Classically activated (M1) macrophages protect from infection but can cause inflammatory disease and tissue damage while alternatively activated (M2) macrophages reduce inflammation and promote tissue repair. Modulation of macrophage phenotype may be therapeutically beneficial and requires further understanding of the molecular programs that control macrophage differentiation. A potential mechanism by which macrophages differentiate may be through microRNA (miRNA), which bind to messenger RNA and post-transcriptionally modify gene expression, cell phenotype and function. The inflammation-associated miRNA, miR-155, was rapidly up-regulated over 100-fold in M1, but not M2, macrophages. Inflammatory M1 genes and proteins iNOS, IL-1b and TNF-a were reduced up to 72% in miR-155 knockout mouse macrophages, but miR-155 deficiency did not affect expression of genes associated with M2 macrophages (e.g., Arginase-1). Additionally, a miR-155 oligonucleotide inhibitor efficiently suppressed iNOS and TNF-a gene expression in wild-type M1 macrophages. Comparative transcriptional profiling of unactivated (M0) and M1 macrophages derived from wild-type and miR-155 knockout (KO) mice revealed an M1 signature of approximately 1300 genes, half of which were dependent on miR-155. Real-Time PCR of independent datasets validated miR-155's contribution to induction of iNOS, IL-1b, TNF-a, IL-6 and IL-12, as well as suppression of miR-155 targets Inpp5d, Tspan14, Ptprj and Mafb. Overall, these data indicate that miR-155 plays an essential role in driving the differentiation and effector potential of inflammatory M1 macrophages.

overall_design: Total RNA was prepared from bone marrow-derived macrophages of miR-155 knockout mice (n=2 independent mice) treated in M0, M1 or M2 conditions (n=2  replicates per condition originating from different mice)

last: Guerau-de-Arellano


title: GE/miRNA expression profile of PBMCs in healthy subjects and MS patients after extra virgin olive oil (EVOO) intake

first: Antonio

last: Moschetta

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


title: Notch induced changes in gene expression in NRK52-cells

status: Public on Jul 01 2016

city: Halle

first: Bayram

last: Edemir

address: Ernst-Grube-Str. 20

institute: University Hospital Halle (Saale)

summary: Overexpression of intracellular domain(NICD) of Notch1 affected the expression level of more than 1000 genes

overall_design: 6 samples were analyzed


title: Gene expression in Src-/- RAW264.7 cells infected with VSV and HSV-1

city: Shanghai

first: Taoyong

address: 800 Xiangyin Road

institute: Second Military Medical University

summary: The purpose of this study was to determine what are the effects of Src deficiency on innate antiviral response upon virus infection in RAW264.7 cells. Wild type and Src-/- RAW264.7 cells were infected with vesicular stomatitis virus (VSV) or herpes simplex virus 1 (HSV-1) for 6h. Then the differentially regulated genes were analyzed.

overall_design: Wild type and Src-/- RAW264.7 cells were infected with vesicular stomatitis virus (VSV, MOI=1) or herpes simplex virus 1 (HSV-1, MOI=5) for 6h. Equal amounts of RNA were assayed for gene expression using Affymetrix mouse 430 2.0 arrays.

first: Zhou

last: Yu

first: Xuelian

first: Xuetao

last: Cao


title: Immediate dysfunction of vaccine-elicited CD8+ T cells primed in the absence of CD4+ T cells

city: Oxford

first: Nicholas

last: Provine

state: Oxfordshire

address: John Radcliffe Hospital

department: NDM - Experimental Medicine

institute: University of Oxford

summary:
CD4+ T cell help is critical for optimal CD8+ T cell expansion after priming in many experimental systems. However, a role for CD4+ T cells in regulating the initial steps of CD8+ T cell effector differentiation is not well established. Here we demonstrate that absence of CD4+ T cells at the time of replication-incompetent adenovirus vector immunization of C57BL/6 mice led to immediate CD8+ T cell dysfunction characteristic of exhaustion at the first detectable timepoints as well as impaired expansion of antigen-specific CD8+ T cells. The absence of CD4+ T cell help resulted in antigen-specific CD8+ T cells that had reduced ex vivo cytotoxicity and decreased capacity to produce IFN-γ and TNF-α. CD8+ T cells primed in the absence of CD4+ T cells expressed elevated levels of the inhibitory receptors PD-1, LAG-3, and Tim-3, and these cells exhibited transcriptomic exhaustion profiles by gene set enrichment analysis. This dysfunctional state was imprinted within 3 days of immunization and could not be reversed by provision of CD4+ T cell help after priming. Partial rescue of unhelped CD8+ T cell expansion and effector differentiation could be achieved by PD-1 pathway blockade or recombinant IL-2 administration.
This study identifies a novel, previously undescribed role of CD4+ T cells to prevent immediate dysfunction and features of exhaustion in CD8+ T cells following antigen priming.

overall_design: Splenic AL11-specific CD8 T cells from mice immunized with Ad5HVR48(1-7)-SIV Gag and treated with anti-CD4 antibody or not were purified by FACS on day 14 post-immunization

first: Dan

middle: H

last: Barouch


title: E2f regulation of gene expression in the liver  [12 mo]

first: Lindsey

last: Kent

state: oh

address: 460 W 12th Ave

department: CCC

institute: OSU

summary:
E2F’s are regulators of the cell cycle and are involved in development and hepatocellular carcinoma. In this study we examine transcriptional changes occurring the liver in E2f1 (1KI) and E2f3b (3bKI) knock in mice. These mice have E2f1 or E2f3b knocked into the E2F3a locus resulting in loss of E2f3a and expression of E2f1 or E2f3b from the E2f3a locus as originally described In Tsai et. al., Nature 2008.
Microarrays were used to evaluate transcriptional changes in spontaneous hepatocellular carcinoma that arose due to alterations in E2F expression.

overall_design: Affymetrix microarrays were performed using mRNA samples from 12 month old livers from wildtype (wt), E2F3a knockout (3aKO) E2f1 knock-in (1KI) and E2f3b knock-in (3bKI) mice. Wt and 3aKO samples were from normal liver and 1KI and 3bKI samples were from spontaneously occurring hepatocellular carcinoma.

first: Gustavo

last: Leone


title: E2f regulation of gene expression in the liver [1 mo]

summary:
E2Fs are regulators of the cell cycle and are involved in development. In this study we examine transcriptional changes occurring the liver in E2f1 (1KI) and E2f3b (3bKI) knock in mice. These mice have E2f1 or E2f3b knocked into the E2F3a locus resulting in loss of E2f3a and expression of E2f1 or E2f3b from the E2f3a locus as originally described In Tsai et. al., Nature 2008.
Microarrays were used to evaluate transcriptional changes due to alterations in E2F expression during liver development.

overall_design: Affymetrix microarrays were performed using RNA samples from 4 weeks (1 month)  old livers from wildtype (wt), E2F3a knockout (3aKO) E2f1 knock-in (1KI) and E2f3b knock-in (3bKI) mice.


title: Expression data of preneoplastic lung neuroendocrine cells and L-Myc signature

first: Youngchul

last: Kim

address: 12902 Magnolia Dr

institute: H. Lee Moffitt Cancer Center

summary: To identify the global gene expression changes driven by L-Myc during SCLC development, mRNA expression profiles were compared using total RNAs from preneoplastic precursors of SCLC and the cells transformed by overexpression of L-Myc.

overall_design: Gene expression microarays of preneoplastic precursor cells of SCLC (preSC) and L-Myc-, C-Myc-, and N-Myc-overexpressing preSCs with biological replicates

first: Kwon-Sik

last: Park

first: Dong-Wook


title: Transcriptomic analysis of two human non-small-cell lung cancer cell lines in response to SN1 methylating-agents treatment

status: Public on Jun 30 2016

city: Athens

first: Olga

last: Papadodima

address: 48, Vasileos Konstantinou av.

country: Greece

institute: National Hellenic Research Foundation

summary: Methylating agents of SN1 type constitute a widely used class of anticancer drugs, the effect of which on human non-small-cell lung cancer (NSCLC) has not been adequately studied. We thus studied the effect of N-methyl-N-nitrosourea (MNU), a model SN1 methylating agent, on two human NSCLC cell lines: A549 (p53wt) and H157 (p53null). We investigated the mechanism of MNU-induced cell death through a time course gene expression profiling study, 24, 48 and 72h following treatment.

overall_design: Two human NSCLC cell lines (A549, H157) were treated with MNU or DMSO for 24h, 48h, or 72h. 34 total samples were analyzed.

first: Panagiotis

last: Moulos

first: Aggeliki

last: Koryllou

first: Fragiskos

last: Kolisis

first: Aristotelis

last: Chatziioannou

first: Vasiliki

last: Pletsa


title: Identification of molecular controls of Corticothalamic projection neurons differentiatiion

status: Public on Jun 28 2016

first: Vibhu

last: Sahni

address: 7 Divinity Avenue

institute: Harvard University

summary:
Molecular mechanisms controlling specification and differentiation of distinct neuron subtypes in the cerebral cortex are not well understood. Corticothalamic projection neurons (CThPN) are a diverse set of neurons, critical for function of the neocortex, but little is known about the molecular mechansims controlling their development.
We used microarrays to detail CThPN gene expression at 3 developmental time points. We then compared CThPN gene expression, with the gene expression of other neuron subtypes in the cerebral cortex at the same stages (previously described in Arlotta et a., 2005)

overall_design: CThPN were retrogradely label with fluorescent microespheres injected into the thalamus, and were FACS purified at 3 developmental stages for RNA extraction and hybridization on Affymetrix microarrays.

first: Maria

last: Galazo

first: Jason

last: Emsley

first: Jeffrey

middle: D

last: Macklis


title: Whole-transcript expression data from normal and DLBCL human peripheral blood samples

city: Rennes

first: Delphine

last: Rossille

address: 2 avenue du Pr. Léon Bernard

institute: INSERM U1236-MOBIDIC

summary:
Gene expression profiling based classification of DLBCL patients versus healthy donors provides insights on transcriptional regulation processes.
Within the most represented pathways in DLBCL, we identified an innate immune response signature, as well as an anti-inflammatory response. On the other hand, a significant under-representation of pathways involved in T-cell activation was also revealed.

overall_design: Whole blood from 76 DLBCL patients and 87 healthy donors was collected into PAXgene Blood RNA tubes (Becton Dickinson BD Biosciences, San Jose, CA, USA) ensuring blood stabilization and stored at -80°C before RNA extraction.  Total RNA, after globin mRNA depletion, was hybridized onto Affymetrix GeneChip® Human Exon 1.0 ST oligonucleotide arrays (Affymetrix, Santa Clara, CA, USA) according to manufacturer’s instructions.

first: Céline

last: Pangault

first: Thierry

last: Fest


title: Selective Akt inhibition by MK-2206 eleminates colorectal cancer-initiating stem cells

city: Frankfurt

first: Patrizia

last: Malkomes

address: Theodor-Stern-Kai 7

institute: University hospital frankfurt

summary:
To identify the regulatory mechanisms and signalling pathways involved in colorectal cancer (CRC) development, we compared the transcriptome of patient-derived tumor-initiating cells (TICs) with their normal stem cell counterparts of the same patient.
This study demonstrates the relevance of AKT-signalling in colonic TIC proliferation and survival. Functional testing uncovered the selective AKT-inhibitor MK-2206 as a potential therapeutic for TIC-directed therapy in CRC.

overall_design: Gene expression profiling of tumor and normal tissues from 5 patients.

first: P

first: M

last: Rieger

first: E

last: Oppermann


title: Expression data from peritoneal macrophages stimulated with lipid A

status: Public on Jun 27 2016

city: Bunkyo-ku

first: Rumi

last: Hachiya

state: Tokyo

address: 1-5-45 Yushima

department: Molecular Endocrinology and Metabolism

institute: Tokyo Medical and Dental University

summary:
Setdb1 is one of the H3K9 methyltransferases and represses gene expression by H3K9 methylation. In an attempt to elucidate the role of Setdb1 in the TLR4-mediated inflammatory responses, we performed DNA microarray analysis using lipid A (the active component of LPS)-stimulated peritoneal macrophages from macrophage specific Setdb1 KO (KO) and WT mice.
The genes upregulated by lipid A treatment in WT macrophages and further increased in KO macrophages contain many genes associated with interleukins and chemokines.

overall_design: Peritoneal macrophages from WT and KO mice were stimulated with lipid A 10 ng/ml or vehicle for 4 h. Microarray analysis was performed using Affymetrix Mouse 430 2.0.

first: Yoshihiro

last: Miyamamoto

first: Takayoshi

last: Suganami

last: Ogawa


title: Adverse Health Effects of Cylindrospermopsin in Laboratory Animal (Mouse) Studies in Single Day Study using Affymetrix Array

status: Public on Jun 24 2016

city: RTP

first: Neil

last: Chernoff

state: NC

address: 109 TW Alexander Dr

institute: US EPA

summary: The goal of this project was to determine gene expression changes in the liver at different times post treatment with the common freshwater cyanobacterial toxin, cylindrospermopsin (CYN).  The liver is generally considered to be the primary target of this toxin and all the data has been derived from livers of exposed animals as well as concurrent controls.  Preliminary gene expression effects have been reported (Chernoff et al., 2010) and the current data extend the time course from 1 hour post exposure to 1-day post cessation of a 5-day period dosing period.

overall_design: Gene expression changes were determined in the livers of pregnant mice exposed to toxic levels of cyanobacterial toxin, cylindrospermopsin.  Animals were exposed to a dose of CYN that elicited significant hepatic toxicity.  This single dose study analyzed liver samples collected at 1, 3, 6, 12 and 24 hours post dose. Gene expression changes were analyzed on the GeneChip® Mouse Genome 430 2.0 Array.


title: Expression data analysis of murine pulmonary cryptococcosis induced by Cryptococcus gattii and Cryptococcus neoformans

status: Public on Jun 22 2016

city: Yokohama,

first: Yoichiro

last: Okubo

state: Kanagawa

address: 2-3-2, Nakao, Asahi-Ku

department: Pathology

institute: Kanagawa Cancer Center

summary: Our previous investigation indicated that high-virulence C. gattii (C. gattii R265) tend to reside in the alveoli, whereas low-virulence C. gattii (C. gattii 5815) tend to be washed out from the alveoli and move into the central side of the respiratory system of the mice. Furthermore, C. gattii R265 and 5815 infected mice showed much lesser macrophage response than C. neoformans H99 infected mice. To elucidate the mechanism of this phenomenon from the viewpoint of genetic analysis, we performed this microarray assay.

overall_design: C. gattii R265, C. gattii 5815, and C. neoformans H99 were prepared for the study. The mice were anesthetized and the spore suspension was intratracheally injected into each mouse. Mice were sacrificed 15 days after the infection and then examined. Lungs of the mice infected with C. gattii R265 (n=4), C. gattii 5815 (n=4), and C. neoformans H99 (n=3) and of a normal control (n=1) were obtained. RNA targets preparation was performed according to the manufacturer's protocol using GeneChip(R) 3' IVT Express Kit (Affymetrix). One hundred nanograms of total RNA were converted into double-stranded cDNA template for transcription. In vitro transcription synthesized amplified RNA (aRNA) and incorporated a biotin-conjugated nucleotide. After purification and fragmentation of aRNA, 12.5 ug of them was hybridized to GeneChip(R) Mouse Genome 430 2.0 Array (Affymetrix).The Probe Array was scanned using a GeneChip(R) Scanner 3000 7G.

first: Y

first: H

last: Ohno

last: Shinozaki

first: T

last: Ishiwatari


title: Image based identification and targeting of cancer stem cells in pancreatic adenocarcinoma

status: Public on Jun 15 2016

city: La Jolla

first: Roman

last: Sasik

state: CA

address: 9500 Gilman Dr.

department: Center for Computational Biology and Bioinformatics

institute: UCSD

summary:
Pancreatic intraepithelial neoplasia (PanIN) is a premalignant lesion that can progress to pancreatic ductal adenocarcinoma, a highly lethal malignancy marked by its late stage at clinical presentation and profound drug resistance. Here we developed novel fluorescent reporter mice that show that the stem cell determinant, Musashi (Msi) is a critical element of pancreatic cancer progression.
These reporters allowed functional and image based tracking of stem cell signals within cancers in vivo, revealing that Msi expression rises as PanINs progress to adenocarcinoma, and that Msi reporter+ tumor cells are the key drivers of pancreatic cancer.

overall_design:
To visualize and track the function of live Msi-expressing cells in vivo, we developed Msi knock-in reporters in which fluorescent signals reflected endogenous Msi expression.
This dataset represents pancreatic cancer_wt and pancreatic cancer_KO cells.  Three wt reps and three KO reps.

first: Raymond

last: Fox


title: Expression data from CD8alpha positive dendritic cells

status: Public on Jun 10 2016

city: Kumamoto

first: Hiroyuki

last: Oshiumi

address: 1-1-1 Honjo Chuo-ku

institute: Kumamoto University

summary:
We screened a number of interferon inducible genes that may be involved in impeding HBV replication and found an anti-HBV activity in ISG20. ISG20 is an IFN-inducible 3’- to 5’-exonuclease, that degrades DNA and RNA and reduces antigen production in hepatocyte-derived cells
A range of candidate genes whose expression was dependent on type I IFN stimulation were identified by gene arrays

overall_design: Total RNA from CD8α+ DCs was extracted from mouse spleens 8h after polyI:C (50 μg) stimulation by RNeasyTM kit. Total RNA (10 μg) from each sample was used to prepare cRNA. Gene expression was analyzed with GeneChipTM

first: Tsukasa

last: Seya


title: Expression profiling of murine leukemia stem cell (LSC) lines established ex vivo by coexpression of R882H-mutated DNMT3A and NRAS-G12D post treatment with Dot1l inhibitor (Microarray)

status: Public on Jun 23 2016

city: Birmingham

first: Rui

last: Lu

state: AL

address: 1824 6th Ave S

institute: Univ of Alabama at Birmingham

summary:
DNA Methyltransferase 3A (DNMT3A) is frequently mutated in various hematopoietic malignancies; however, the underlying oncogenic mechanisms remain elusive. Here, we report that DNMT3A mutational ‘hotspot’ at Arg882 (DNMT3A-R882H) cooperates with constitutively activated RAS in transforming murine hematopoietic stem/progenitor cells (HSPCs) ex vivo and inducing acute leukemias in vivo. DNMT3A-R882H potentiates aberrant transactivation of ‘stemness’ gene expression programs, notably transcription factors Meis1, Hox-A, Mn1 and Mycn. Mechanistically, R882-mutated DNMT3A directly binds to cis-regulatory elements of these genes and induces focal CpG hypomethylation reminiscent of what was seen in human leukemias bearing DNMT3A R882 mutation. Furthermore, DNMT3A-R882H induced DNA hypomethylation facilitates gene enhancer/promoter activation and recruitment of Dot1l-associated transcription elongation machineries. Inactivation of Dot1l represses DNMT3AR882H-mediated stem cell gene dysregulation and acute leukemogenicity.

In this dataset, we provided gene expression profiling data for (1) RH-RAS leukemia stem cells (RH-RAS LSCs), (2) LSCs transformed by MLL-AF9, (3) LSCs transformed by NUP98-JARID1A, and (4) Dot1l inhibitor-treated RH-RAS LSCs.

overall_design: Gene expression data were generated using Mouse Genome 430 2.0 Microarray (Affymetrix) for four independently derived RH-RAS LSC lines (termed as LSC RH-RAS #1, #2, #3 and #4), two RH-RAS LSC lines (LSC RH-RAS #1 and # 3) treated with 1 µM SGC0946 (a Dot1l-specific small-molecule inhibitor) for 4 days, one MLL-AF9-transformed progenitor line and three NUP98-JARID1A transformed progenitor lines.

first: Gang

last: Wang


title: Chronic Restraint Stress Upregulates Erythropoiesis Through Glucocorticoid Stimulation

status: Public on Jun 07 2016

city: Indianapolis

first: Leni

last: Moldovan

state: IN

address: 980 W Walnut St., Rm. C422

department: Ophthalmology

institute: Indiana University

summary: In response to elevated glucocorticoid levels, erythroid progenitors rapidly expand to produce large numbers of young erythrocytes. Previous work demonstrates hematopoietic changes in rodents exposed to various physical and psychological stressors, however, the effects of chronic psychological stress on erythropoiesis has not be delineated. We employed laboratory, clinical and genomic analyses of a murine model of chronic restraint stress (RST) to examine the influence of psychological stress on erythropoiesis. Mice exposed to RST demonstrated markers of early erythroid expansion involving the glucocorticoid receptor. In addition, these RST-exposed mice had increased numbers of circulating reticulocytes and increased erythropoiesis in primary and secondary erythroid tissues. Mice also showed increases in erythroid progenitor populations and elevated expression of the erythroid transcription factor KLF1 in these cells. Together this work describes some of the first evidence of psychological stress affecting erythroid homeostasis through glucocorticoid stimulation and begins to define the transcription factor pathway involved.

overall_design: RNA was extracted from thwe whole blood of RST mice (n = 4) and Control mice (N = 4) following seven days of restraint stress.

first: Jeffrey

middle: L

last: Voorhees

first: Nicole

last: Powell

first: Xiaoku

last: Mo

first: Timothy

last: Eubank

first: Clay

middle: B

last: Marsh


title: Identification and targeting of long-term tumor propagating cells in small cell lung cancer

city: Stanford

first: Julien

last: Sage

address: 265 Campus Drive, SIM1 G2078

department: Pediatrics

institute: Stanford University

summary:
FACS sorted TPCs (CD24HighCD44LowEpCAMHigh) and non-TPCs (CD24Low, CD24HighCD44High, and CD24HighCD44LowEpCAMLow) from mouse primary SCLC tumors
We used microarrays to identify genes that are differentially expressed in TPCs versus non-TPCs.

overall_design: Tumors isolated and dissociated from the mouse SCLC pre-clinical model and single cell suspension stained with cell surface markers (CD24, CD44, and EpCAM)

first: Nadine

last: Jahchan


title: Expression data from SHP specific siRNA or nonspecefic siRNA transfected rat astrocytes [extended study]

status: Public on Jun 04 2016

city: Suwon

first: jeehoon

last: lee

state: Gyoungido

address: San5, Woncheondong

department: Pharmacology

country: South Korea

institute: Ajou university, School of Medicine

summary: To clarify the effect of SHP in LXRs-mediated signaling pathway, we performed global gene expression analysis of SHP siRNA transfected- or control siRNA transfected- astrocytes after IFN-γ and LXRs agonist. Microarray analysis revealed that expression of several genes encoding inflammatory mediators were reversed in SHP siRNA transfected-astrocytes, when compared with control siRNA transfected-astrocytes.

overall_design:
Primary astrocytes were cultured from the cerebral cortices of 1 day-old Sprague-Dawley rats. The astrocytes transfect with control siRNA or SHP siRNA and treated withIFN-γ in the presence or absence of GW for 3 h.

This study includes a re-analysis of GSM2036031, GSM2036032, GSM2036033, and GSM2036034 from GSE76704.

first: Jeehoon

last: Lee

first: Ilo

last: Jou


title: Polysomal and total RNA in controls and after 10 min global brain ischemia and 8 hours of reperfusion

status: Public on Jun 02 2016

city: Detroit

first: Donald

middle: James

last: DeGracia

address: 540 E. Canfield

department: Physiology

institute: Wayne State University

summary:
Complete global brain ischemia (CGBI) and reperfusion occur following resuscitation from cardiac arrest.  Different brain neurons are selectively vulnerable to CGBI: pyramidal neurons of hippocampal CA3 survive 10 min CGBI but those of CA1 die at 3 days following 10 min CGBI. CA3 neurons are expected to have more robust stress responses and repair responses than CA1 neurons.
We used microarrays to compared total and polysome-bound mRNAs in CA1 and CA3 at 8 hr reperfusion after 10 min CGBI in Long Evans male rats to ascertain differences in total vs polysome-bound gene expression.

overall_design: Male Long Evans rats were subjected to (1) sham operation (non-ischemic control, NIC) or normothermic CGBI of 10 min followed by 8 hr reperfusion (8R). Hippocampal CA1 and CA3 were dissected. n = 5 CA1 or CA3 were pooled to give a single replicate and there were 3 or 4 replicates per group. Post-mitochondrial supernatant (PMS) was prepared. Twenty percent of PMS was TRIzol extracted to give total RNA. The remainder was run on a 20% sucrose pad to isolate polysome pellets, which were also TRIzol extracted to give polysome RNA.  Total and polysome RNA were then run on Affymetrix Rat Gene 2.0 microarrays.

middle: J

first: Fika

last: Anggraini

first: Haihui

first: Xuequn

last: Chen


title: Adverse Health Effects of Cylindrospermopsin in Laboratory Animals (mouse) Studies

first: Neil

last: Chernoff

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

overall_design: Refer to individual Series