title: Control of LPS induced gene expression in bone marrow derived macrophages by the p50/p105 subunit of NF-kB and IL-10

first: Bruce

last: Horwitz

address: 77 Avenue Louis Pasteur

institute: Brigham and Women's Hospital

summary: Bone marrow-derived macrophages were produced from mice lacking IL-10 alone (IL10-def) or mice lacking both IL-10 and the p50/p105 subunit of NF-kB (p50/IL10), and left unstimulated, stimulated with LPS (1 ng/ml) or stimulated with LPS and IL-10 (0.3 ng/ml).

overall_design: There are 12 total samples, with 2 each from the groups described in the summary.  Pairwise comparisons between groups were evaluated.


title: Chromatin remodeling enzyme Brg1 is required for mouse lens fiber cell terminal differentiation and their denucleation

status: Public on Jan 01 2011

city: LYON

first: Jiri

last: ZAVADIL

state: Other

address: 150 COURS ALBERT THOMAS

country: France

institute: IARC WHO

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

overall_design: Refer to individual Series


title: Gene expression changes in femur bone induced by skeletal muscle unloading

status: Public on Dec 21 2010

city: Sharnbrook

first: Fei Ling

last: Lim

state: Bedfordshire

address: Colworth Science Park

country: United Kingdom

institute: Unilever

summary: Gene expression changes in femur bone induced by acute skeletal muscle unloading, which leads to physiological changes including muscle atrophy, weakness and results in bone remodelling and subsequent loss of bone mass, was investigated by hind-limb suspension (HLS) treatment of Male ICR mice (28–32 g body wt; Harlan, Indianapolis, IN). AgilentTM Whole Mouse Genome Oligo Microarrays were utilised to examine the effects of HLS on mRNA expression profiles of the femur bone in the hindlimbs of freely ambulating control and 24h HLS treated mice. Five independent biological replicates of this experiment were carried out.

overall_design: Five independent biological replicates of this experiment (Control and HLS) were carried out.

first: Dawn

middle: J

last: Mazzatti

first: Melissa

middle: A

last: Smith

first: Kavita

last: Karnik

first: Fei-Ling

first: John

last: Williams

first: Michael

middle: B

last: Reid


title: Expression profiles of the hippocampus of Rsk2-KO mice

status: Public on Dec 22 2010

city: Illkirch

first: André

last: Hanauer

address: 1, rue laurent Fries

department: Neurobiology and Genetics

institute: IGBMC

summary:
Coffin–Lowry Syndrome (CLS) is a syndromic form of mental retardation caused by loss of function mutations in the X-linked RPS6KA3 gene, which encodes Rsk2, a serine/threonine kinase involved in spatial memory. We analyzed hippocampal gene expression profiles  in Rsk2-KO mice to identify changes in molecular pathways.
Total RNA was extracted from hippocampi from 6 KO and 6 WT (littermates) 2-month-old male mice. For each genotype, equivalent amounts of RNA from 2 mice were pooled and processed for hybridization to the genome wide oligonucleotide microarray (Murine 430A 2.0 Affymetrix, 22.000 probe sets). Thus, 3 independent pooled samples were hybridized for each genotype.

overall_design: We compared hippocampal gene expression profiles from rsk2-KO and normal littermate mice to identify changes in molecular pathways

first: Tahir

last: Mehmood

first: Anne

last: Schneider

first: Jérémie

last: Sibillec

first: Patricia

last: Marques-Pereira

first: Solange

last: Pannetier

first: Mohamed

last: Ammar

first: Doulaye

last: Dembele

first: Christelle

last: Thibault-Carpentier

first: Nathalie

last: Rouach


title: Expression data of mouse fetal liver during embryonic day 18 and 19

status: Public on Oct 01 2011

city: Wuhan

first: Xiaodong

last: Li

state: Hubei Province

address: Luojia Hill, Wuchang District

department: College of Life Sciences

country: China

institute: Wuhan University

type:
Expression profiling by array
Third-party reanalysis

summary:
The oscillation status of the circadian clock during late gestation is not clear. To gain a better understanding on the oscillation state of the clock and possible influences by maternal cues, we performed transcriptome analyses on the fetal liver tissue during late gestation.
Fetal liver transcriptome data were analyzed and compared to adult mouse data in the public database: GSE11923 and GSE13093 (only samples GSM327130 to GSM327141).  Re-analyzed (gc-RMA) data from GSE11923 and GSE13093 linked below as supplementary files.

overall_design: Fetal mouse liver tissues were collected at four hours intervals across embryonic day 18 and day 19. Groups 1 and 2.

first: Chengwei


title: Lungs of mice exposed to subtoxic doses of nano-titanium dioxide particles by inhalation

status: Public on Dec 13 2010

city: Ottawa

first: Andrew

state: ON

address: 50 Columbine

country: Canada

institute: Health Canada

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

summary:
Acute phase reactants serum amyloid A-1, 3 and micro RNA-135b, -449a, and -1 are induced in lungs of mice exposed to subtoxic doses of nano-titanium dioxide particles by inhalation
In the present study we investigate pulmonary mRNA and miRNA profiles of mice exposed to subtoxic dose of nano-titanium dioxide particles by inhalation. We show dramatic induction of acute phase reactants, chemoattractants, immune and host defence related genes. We also demonstrate for the first time changes in miRNA profiles in the lungs in response to nanoTiO2.

Keywords: Toxicology, disease state analysis, biomarkers of health effects

overall_design: Female C57BL/6 mice were exposed to 40 mg nanoTiO2/m3 for one hour/day for 11 consecutive days and were sacrificed 5 days following the last exposure. Left lung lobes and liver were removed and flash frozen. Total RNA was isolated from a small random part of the frozen lung and liver and was hybridized against universal mouse reference RNA to Agilent Oligo DNA microarrays (Agilent Technologies) containing 44,000 transcripts. Microarrays were normalized using a global LOWESS approach and analyzed by MAANOVA 2.0 and SAM. Microarray results were validated by real time RT-PCR. Impact of alteration in expression of select genes was further validated by analysing their total protein levels in lung tissue homogenates.

first: Sabina

last: Halappanavar

first: Petra

last: Jackson

first: Karin

middle: S

last: Hougaard

first: Ulla

last: Vogel

first: Carole

middle: L

last: Yauk

first: Håkan

last: Wallin


title: Chromatin remodeling enzyme Brg1 is required for mouse lens fiber cell terminal differentiation and their denucleation [lens tissue]

first: Jiri

last: ZAVADIL

summary:
Genome-wide approach to identify the cell-autonomous role of Brg1 in lens fiber cell terminal differentiation.
To examine roles of Brg1 in mouse lens development, a dnBrg1 transgenic construct was expressed using the lens-specific alphaA-crystallin promoter in postmitotic lens fiber cells. Morphological studies revealed abnormal lens fiber cell differentiation in transgenic lenses resulting in cataract. Electron microscopic studies showed abnormal lens suture formation and incomplete karyolysis (denucleation) of lens fiber cells. To identify genes regulated by Brg1, RNA expression profiling was performed in E15.5 embryonic wild type and dnBrg1 transgenic lenses. In addition, comparisons between differentially expressed genes in dnBrg1 transgenic, Pax6 heterozygous, and Hsf4 homozygous lenses identified multiple genes co-regulated by Brg1, Hsf4 and Pax6. Among them DNase IIbeta, a key enzyme required for lens fiber cell denucleation, was found downregulated in each of the Pax6, Brg1 and Hsf4 model systems. Lens-specific deletion of Brg1 using conditional gene targeting demonstrated that Brg1 was required for lens fiber cell differentiation and indirectly for retinal development but was not essential for lens lineage formation.

overall_design: Wild type and dnBrg1 transgenic lenses, 4 biological replicates each

first: Shuying

last: He

first: Melinda

last: Pirity

first: Wei-Lin

last: Wang

first: Louise

last: Wolf

first: Bharesh

middle: K

last: Chauhan

first: Kveta

last: Cveklova

first: Akira

last: Nakai

first: Ernest

middle: R

last: Tamm

first: Ruth

last: Ashery-Padan

last: Zavadil

first: Ales

last: Cvekl


title: Gene expression profiles of Lkb1 WT and KO hematopoietic stem cells (HSCs)

status: Public on Dec 01 2010

city: Houston

first: Sujun

last: Hua

state: Tx

address: 1901 East Rd

country: USA

institute: MD Anderson Cancer Center

summary: LKB1 encodes a Ser/Thr kinase and acts as an evolutionarily conserved sensor of cellular energy status in eukaryotic cells. LKB1 functions as the major upstream kinase to phosphorylate AMPK and 12 other AMPK-related kinases, which is required for their activation in many cellular contexts. Once activated, AMPK and AMPK-related kinases phosphorylate a diverse array of downstream effectors to switch on ATP-generating catabolic processes and switch off ATP-consuming anabolic processes, thus restoring energy balance during periods of energetic stress. To study the role and mechanisms of Lkb1 in the regulation of hematopoietic stem cell (HSC) biology, we performed transcriptome analysis of sorted LSK (Lin-, Sca-1+, c-Kit+) cells from Lkb1 WT and KO bone marrows at 1 day post-completing tamoxifen injection (DPI). To identify more proximal molecular effects, we chose 1 DPI due to the modest phenotypes in Lkb1 KO mice, yet documentation of efficient Lkb1 deletion in LSK cells at this very early time point.

overall_design: We treated Lkb1 L/L rosa26CreERT2 and Lkb1 L/L mice (C57BL/Ka-CD45.2:Thy-1.1 background) with Tamoxifen for 5 days to somatically delete Lkb1 in adult mice, and generated Lkb1 WT and KO mice.  At 1 DPI, we prepared single-cell suspensions from bone marrow (from femoral and tibial bones), and stained and sorted LSK populations using FACSAria (Becton Dickinson, Mountain View, CA). The RNA was extracted from sorted LSK cells, amplified and subjected to gene profiling. The samples include 3 Lkb1 WT (Lkb1 WT 5-7) and 4 Lkb1 KO (Lkb1 KO 4-7) replicates.

first: Boyi

last: Gan

first: Ron

last: DePinho


title: Epistasis analysis of Runx1 and Gata1 over HoxA3 in hemogenic endothelium

status: Public on Dec 20 2010

city: Minneapolis

first: Michael

last: Kyba

state: MN

address: 312 Church St. SE

institute: University of Minnesota

summary: We observe that HoxA3 represses hematopoieis by the repression of several transcription factors including Runx1 and Gata1. Up regulation of either Runx1 or Gata1 in the presence of HoxA3 reverted the hematopoietic repression. We have performed full genome analysis to determine the molecular signature of hematopoietic development in response to upregulation of Runx1 and Gata1.

overall_design: Endothelial progenitors were sorted from HoxA3 induced EBs, transduced with either control vector (control), Runx1 vector or Gata1 vector. Cells were co-cultured on Op9 for 5 days: in the following conditions: Control, HoxA3 upregulation, HoxA3 + Runx1 upregulation, HoxA3 + Gata1 upregulation in triplicate. After 5 days of culture,transduced cells were sorted (5000 cells) and prepared for microarray.

first: Michelina

last: Iacovino


title: HoxA3 is an apical regulator of hemogenic endothelium

first: Istvan

last: Szatmari


title: Expression data from WT or p65-/- mouse embryonic fibroblasts (MEFs) infected with Toxoplasma gondii.

status: Public on Jan 10 2011

city: Cambridge

first: Emily

middle: E

last: Rosowski

state: MA

address: 77 Massachusetts Ave, 68-258d

department: Biology

institute: MIT

summary:
Toxoplasma strains have been shown to modulate host cell transcription.  We have found a type II Toxoplasma gene, GRA15, which activates the nuclear translocation of the NF-kappaB p65 transcription factor.
We used microarrays to determine how GRA15II modulates host cell transcription, and whether this transcription is dependent on the p65 transcription factor.

overall_design: WT or p65-/- MEFs were infected with type I (RH), type I GRA15II (RH GRA15II), type II (Pru), or type II GRA15KO (Pru GRA15KO) parasites for 18-24 hours. Total RNA was isolated and hybridized to Affymetrix GeneChip Human Genome U133A 2.0 arrays.

first: Jeroen

middle: P

last: Saeij


title: Chronic Intermittent Hypoxia Increases Alveolar Surface Area in Adult Mice

status: Public on Dec 31 2010

city: Baltimore

first: Dmitry

middle: N

last: Grigoryev

state: MD

institute: JHU

summary: Obstructive sleep apnea (OSA) leads to increased cardiovascular morbidity and mortality, which have been attributed to intermittent hypoxia (IH). The effects of IH on lung structure and function are unknown. We used a mouse model of chronic IH, which mimics the O2 profile in patients with OSA. We exposed adult C57BL/6J mice to 3 months of IH with an FIO2 nadir of 5%, 60 times/hr during the 12hr light phase. Control mice were exposed to room air.

overall_design: Gene microarrays were performed in a separate subset of animals (IH, n = 5; control, n = 5). Total RNA was isolated from lung tissue using the Trizol Reagent method, gene microarrays were performed with the Affymetrix GeneChip® Mouse Genome 430A 2.0 Array (MG 430A 2.0; Affymetrix, Inc., Santa Clara, CA) and analyzed using Significance Analysis of Microarray (SAM) software.

first: Christian

last: Reinke


title: Gene profile analysis of sorted Sca1+/cKit- BMCs obtain from mice bearing instigator, non-instigator  and Matrigel

status: Public on Nov 27 2010

city: Lund

first: Björn

last: Nilsson

address: BMC

department: Hematology and Transfusion Medicine

country: Sweden

institute: Lund University

summary: Sca1+/cKit– hematopoietic BMCs of hosts bearing instigating tumors  (BPLER) promote the growth of responding (HMLER-HR) tumors that form with a myofibroblast-rich, desmoplastic stroma. BMCs from mice bearing Non-instigating tumors lack this ability

overall_design: Sca1+/cKit- BMCs were isolated from mice bearing Matrigel control or size-matched instigating or non-instigating tumors by FACS directly into Trizol reagent (Invitrogen).

first: Ann

middle: M

last: Gifford

first: Bjorn

first: Sandra

last: McAllister

first: Benjamin

last: Ebert


title: Paneth cells constitute the niche for Lgr5 stem cells in intestinal crypts

status: Public on Nov 29 2010

city: Dresden

first: Daniel

middle: E.

last: Stange

address: Fetscherstr. 74

country: Germany

institute: University Clinic Dresden

summary: Homeostasis of self-renewing small intestinal crypts results from neutral competition between Lgr5 stem cells, small cycling cells located at crypt bottoms1, 2. Lgr5 stem cells are interspersed between terminally differentiated Paneth cells, that are known to produce bactericidal products such as lysozyme and cryptdins/defensins3.  Single Lgr5-expressing stem cells can be cultured to form long-lived, self-organizing crypt-villus organoids in the absence of non-epithelial niche cells4. Here, we note a close physical association of Lgr5 stem cells with Paneth cells in vivo and in vitro. CD24+ Paneth cells express EGF, TGFα, Wnt3 and the Notch-ligand Dll4, all essential signals for stem cell maintenance in culture. Co-culturing of sorted stem cells with Paneth cells dramatically improves organoid formation. This Paneth cell requirement can be substituted by a pulse of exogenous Wnt. Genetic removal of Paneth cells in vivo results in the concomitant loss of Lgr5 stem cells. In colon crypts, CD24+ cells residing between Lgr5 stem cells may represent the Paneth cell equivalents. We conclude that Lgr5 stem cells compete for essential niche signals provided by a specialized daughter cell, the Paneth cell.

overall_design: We used intestinal cell fractions from Lgr5-EGFP-ires-CreERT2 mice, expressing GFP under the control of the Lgr5 promoter. RNA was isolated from two FACS sorted cell populations: stem cells were sorted based on high level of GFP expression (GFPhi) and Paneth cells were sorted based on high level of CD24 expression (CD24hi) and high side-scatter (SSChi). Differentially labelled cRNA from GFPhi and CD24hi/SSChi cells from two different sorts (each combining ten individual mice) were hybridized on 4X44K Agilent Whole Mouse Genome dual colour Microarrays (G4122F) in two dye swap experiments, resulting in four individual arrays.

first: Sato

last: Toshiro

first: Hans

last: Clevers


title: Stage-specific sensitivity to p53 restoration in lung cancer

status: Public on Nov 24 2010

first: Charles

middle: Arthur

last: Whittaker

institute: Koch Institute


title: Stage-specific sensitivity to p53 restoration in lung cancer: cell line data

summary: Tumorigenesis is a multistep process that results from the sequential accumulation of mutations in key oncogene and tumor-suppressor pathways. The quest to personalize cancer medicine based on targeting these underlying genetic abnormalities presupposes that sustained inactivation of tumor suppressors and activation of oncogenes are required for tumor maintenance. Mutations in the p53 tumor-suppressor pathway are a hallmark of cancer and significant efforts toward pharmaceutical reactivation of mutant p53 pathways are underway1-3. Here we show that restoration of p53 in established murine lung tumors leads to significant but incomplete tumor cell loss specifically in malignant adenocarcinomas but not in adenomas. Also, we define amplification of MAPK signaling as a critical determinant of malignant progression. The differential response to p53 restoration depends on activation of the Arf tumor suppressor downstream of hyperactive MAPK signaling. We propose that p53 naturally limits malignant progression by responding to increased oncogenic signaling, but is unresponsive to low levels of oncogene activity that are sufficient for early stages of lung tumor development. These data suggest that restoration of pathways important in tumor progression, as opposed to initiation, may lead to incomplete tumor regression due to the stage-heterogeneity of tumor cell populations.

overall_design: 3 cell lines each treated with Tamoxifen or EtOH vehicle. Tamoxifen treatment results in reactivation of p53 expression

first: David

last: Feldser

first: Kamena

last: Kostova

first: Monte

last: Winslow

first: Sarah

last: Taylor

first: Chris

last: Cashman

first: Francisco

last: Sanchez-Rivera

first: Rebecca

last: Resnick

first: Roderick

last: Bronson

middle: T

last: Hemann

first: Tyler

last: Jacks


title: tTA/TDP Mice Expression Array

status: Public on Nov 10 2010

city: Philadelphia

first: Virginia

last: Lee

address: 3rd Floor Maloney Building; 3600 Spruce St

institute: University of Pennsylvania

summary:
Transgenic (Tg) mice expressing nuclear or cytoplasmic human TDP-43 were generated.
Tg mice had motor spasticity and forebrain neurodegeneration.
Human TDP-43 reduced mouse TDP-43 in nuclei of affected neurons.
Tg mice showed alterations in transcripts related to chromatin assembly.

overall_design: Cerebral cortex from 21 transgenic mice and controls were assayed after two weeks off doxycyline diet as described in Igaz et al.


title: mRNA expression profiling in adult mouse liver following benzo(a)pyrene (BaP) treatment [Agilent gene expression array]

status: Public on Oct 18 2010

first: Andrew

last: Williams

summary:
Adult male mice were exposed to 150 mg/kg benzo(a)pyrene (BaP) or solvent for 3 days and sampled 4 or 24 hours after the last dose. mRNA expression levels in adult mouse liver were measured using Agilent arrays. We found widespread changes in mRNA in pathways consistent with known response (xenobiotic metabolism, glutathione). We also found that BaP caused changes in the circadian rhythm pathway. We measured miRNA changes in the same samples and found no evidence for any change in transcription of miRNA as a result of the exposure.

Keywords: Toxicology, time course

overall_design: Adult male B6C3F1 mice were exposed to a daily dose of corn oil (vehicle control group) or 150 mg/kg BaP (treatment group) for 3 days (n=5 per group). Mice were sacrificed at 4 h or 24 h following the last dose and liver lobes were extracted and flash frozen. RNA was extracted from median liver lobes and hybridized to the Agilent 4 x 44K mouse DNA arrays using a randomized block design.

first: Carole

last: Yauk

first: Morie

last: Molowaney

first: Kelly

last: Jackson

first: Lynn

last: Berndt-Weis


title: Intact ureteric buds gene expression with AngII treatment

status: Public on Nov 01 2010

city: new orleans

first: renfang

last: song

state: LA

address: 1430 tulane ave

institute: tulane university

summary: Compare the gene expression in intact Ubs after treated with AngII vs. Media, determine the key genes related to the ub branching gene expression change pattern.

overall_design: Two condition experiments, media and AngII. Biological replicate. Two for media samples, two for AngII treatment samples.

first: Ihor

last: Yosypiv


title: ShcA is a Paracrine Integrator of the Adaptive Immune Response during Breast Cancer Progression

status: Public on Oct 12 2010

city: Montreal

first: Sean

last: Cory

state: QC

address: 3649 Promenade Sir William Osler

department: Bioinformatics

institute: McGill University

summary: Using transgenic mouse models of breast cancer, we demonstrate that loss of ShcA signaling within mammary tumors results in extensive CD4+ T cell infiltration, activation and induction of a humoral immune response. Our studies reveal that ShcA signaling during early breast cancer progression is required to establish and maintain an immunosuppressive state that favors tumor growth. Consistent with these transgenic studies, high ShcA levels correlate with poor outcome and reduced CTL infiltration in primary human breast cancers. Conversely, elevated expression of a ShcA-regulated immune signature, generated from ShcA-null mammary tumors, is a predictor of good prognosis in HER2-positive and basal breast cancer patients. These observations define a novel role for ShcA in polarizing the immune response to facilitate tumorigenesis

overall_design: NIC SHC null Tumors vs. pooled MMPV-NIC reference, some replicate dye swaps

first: Josie

last: Ursini-Siegel

first: William

last: Muller


title: Adult mouse liver following benzo(a)pyrene (BaP) treatment: miRNA and mRNa profiling

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

platform_organism:
Homo sapiens
Mus musculus
Rattus norvegicus
Human alphaherpesvirus 1
Human betaherpesvirus 5
Murid betaherpesvirus 1
human gammaherpesvirus 4
JC polyomavirus
Human immunodeficiency virus 1
Murid gammaherpesvirus 4
Human gammaherpesvirus 8
Betapolyomavirus hominis
Betapolyomavirus macacae

overall_design: Refer to individual Series


title: Comparison of murine colonic mucosal gene expression between offspring born to mothers fed a methyl donor diet (MD) versus control at postnatal day 90 (P90).

status: Public on Oct 20 2010

first: Richard

last: Kellermayer

state: TX

address: One Baylor Plaza

institute: Baylor College of Medicine

type:
Expression profiling by array
Methylation profiling by array

summary: BACKGROUND & AIMS: Inflammatory Bowel Diseases (IBD), including Crohn’s disease and ulcerative colitis, are chronic illnesses that are thought to develop secondary to a pathologic interaction between the immune system and the intestinal microflora that is manifested by the gut mucosa. IBD has been recognized as disorders in which developmental epigenetic changes, such as DNA methylation, may play an important pathogenic role.  DNA methylation can be influenced in mammals by dietary exposures. A methyl-donor diet has been specifically found to be effective in inducing permanent changes in DNA methylation at certain genomic loci in murine models. Importantly, the methyl-donor substances utilized are routinely incorporated into prenatal micronutrient supplements for humans. In this study we addressed whether maternal exposure to a methyl-donor diet induces prolonged alterations in offspring colitis susceptibility and whether it leads to stable colonic mucosal epigenetic changes and gene expression alterations in mice. We also assessed whether the maternal methyl-donor diet induced persistent changes in the colonic microbiota in the offspring.  METHODS: Colonic mucosa from offspring of mothers fed a methyl donor diet (MD) or control diet was interrogated by methylation specific amplification microarray (MSAM) at postnatal day 30 (P30) and P90 to screen for changes in DNA methylation, with bisulfite pyrosequencing validation. Transcriptomic changes in the same tissue were analyzed by microarray expression profiling and real time RT-PCR. The mucosal microbiome was studied by high throughput, detailed pyrosequencing of 16S rRNA.  RESULTS: MD exposure during prenatal and early development lead to a significant increase in colitis susceptibility that persisted even after 69 days of diet reversal  (P90).  MD exposure also influenced DNA methylation and expression at select genomic loci.  Overlap between DNA methylation and gene expression changes was confirmed at Ppara, a gene previously implicated in murine colitis.  Metagenomic analyses failed to reveal consistent bacteriomic differences between the P30 and P90 age groups. CONCLUSIONS:  Prenatal and early developmental exposure to MD induces increased colitis susceptibility, mucosal epigenomic, and transcriptomic changes that do not appear to associate with consistent microbiomic alterations. These findings underscore the importance of maternal nutrition on offspring colitis susceptibility in mammals and implicate the importance of the associated mucosal epigenetic modification. Our results bare potentially significant public health relevance as well.

overall_design: 4 independent MD versus control comparisons at P90 were performed as follows. RNA (0.4ug) samples were processed and labelled with Cy3 and Cy5 (Quick Amp labelling kit, two color, Agilent technologies)  and 4 independent P90 MD to P90 control comparisons were done on Agilent technologies 4x44k whole genomic expression microarray G2519F, Amadid:014868)

first: Tiffany

middle: D

last: Schaible


title: Role of interleukin-16 in macrophage responses to Tropheryma whipplei and lipopolysaccharide

status: Public on Nov 08 2010

city: Marseille

first: Benoit

last: Desnues

address: 27 boulevard Jean Moulin

department: URMITE UMR CNRS 6236

institute: Faculté de Médecine de la Timone


title: Histone H3K27ac separates active from poised enhancers and predicts developmental state (gene expression data)

status: Public on Oct 31 2010

city: Rotterdam

first: Menno

last: Creyghton

address: Doctor Molewaterplein 40

country: Netherlands

institute: Erasmus MC

summary: Developmental programs are controlled by transcription factors and chromatin regulators, which maintain specific gene expression programs through epigenetic modification of the genome. These regulatory events at enhancers contribute to the specific gene expression programs that determine cell state and the potential for differentiation into new cell types. While enhancer elements are known to be associated with certain histone modifications, and transcription factors, the relationship of these modifications to gene expression and developmental state has not been clearly defined. Here we interrogate the epigenetic landscape of enhancer elements in embryonic stem cells and several adult tissues in the mouse. We find that histone H3K27ac distinguishes active enhancers from inactive/poised enhancer elements, thus providing clues to current cell state and further developmental potential.

overall_design: Gene expression profiling was performed in mouse ES, NPC, liver, and pro-B

first: Albert

middle: W

last: Cheng

first: Rudolf

last: Jaenisch


title: Gene expression profiles in livers caused by Atg7 and/or Nrf2 deficiency

status: Public on Oct 15 2010

city: Sendai

first: Hozumi

last: Motohashi

state: Miyagi

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

department: Center for Radioisotope Science

country: Japan

institute: Tohoku University Graduate School of Medicine

summary:
Autophagy deficiency caused by conditional knockout of Atg7 results in severe hepatitis accompanied by abundant accumulation of p62.
p62 stablizes Nrf2 by disrupting the association between Keap1 and Nrf2.  To understand the pathogenesis of hepatitis under the autophagy deficiency, we examined gene expression profiles of livers from Atg7-null, Nrf2-null and Atg7-Nrf2 double mutant mice.

overall_design: Eight week old Atg7F/F:Mx1-Cre mice and Atg7F/F:Mx1-Cre:Nrf2-/- together with control mice were injected with pIpC. At 4 weeks after pIpC injection, total RNAs were purified from each mouse liver.

first: M

last: Komatsu

first: K

last: Taguchi

first: Y

last: Nishito

first: H

last: Yamamoto


title: Interleukin-16-knock-out bone-marrow derived macrophages response to the Whipple's disease agent, Tropheryma whipplei

status: Public on Oct 08 2010

summary: We have employed whole genome microarray expression profiling to identify differently expressed genes following infection of interleukin-16-knock-out bone-marrow derived macrophages with T. whipplei. Macrophages were infected with T. whipplei (MOI 50:1) for 6 hours and a signature was identified that distinguished between infected and control samples. Expression of several genes from this signature was quantified in the same RNA samples by real-time PCR, confirming the predicted macrophage response pattern.

overall_design: Gene expression in macrophages was measured at 6 hours after stimulation  Three independent experiments were performed.

first: Jean-Louis

last: Mège


title: Interleukin-16-knock-out bone-marrow derived macrophages response to Escherichia coli lipopolysaccharide (LPS)

summary: We have employed whole genome microarray expression profiling to identify differently expressed genes following stimulation of interleukin-16-knock-out bone-marrow derived macrophages with Escherichia coli lipopolysaccharide (LPS). Macrophages were stimulated with LPS (100 ng/ml) for 6 hours and a signature was identified that distinguished between infected and control samples. Expression of several genes from this signature was quantified in the same RNA samples by real-time PCR, confirming the predicted macrophage response pattern.


title: HSF4 microarray gene expression analysis in the newborn mouse lens.

city: LYON

first: Jiri

last: ZAVADIL

address: 150 COURS ALBERT THOMAS

institute: IARC WHO

summary:
Differential expression of HSF4 in null newborn mouse and wildtype lenses was examined to identify putative downstream targets of HSF4.
To examine roles of Brg1 in mouse lens development, a dnBrg1 transgenic construct was expressed using the lens-specific aA-crystallin promoter in postmitotic lens fiber cells. Morphological studies revealed abnormal lens fiber cell differentiation in transgenic lenses resulting in cataract. Electron microscopic studies showed abnormal lens suture formation and incomplete karyolysis (denucleation) of lens fiber cells. To identify genes regulated by Brg1, RNA expression profiling was performed in E15.5 embryonic wild type and dnBrg1 transgenic lenses. In addition, comparisons between differentially expressed genes in dnBrg1 transgenic, Pax6 heterozygous, and Hsf4 homozygous lenses identified multiple genes co-regulated by Brg1, Hsf4 and Pax6. Among them DNase IIb, a key enzyme required for lens fiber cell denucleation, was found downregulated in each of the Pax6, Brg1 and Hsf4 model systems. Lens-specific deletion of Brg1 using conditional gene targeting demonstrated that Brg1 was required for lens fiber cell differentiation and indirectly for retinal development but was not essential for lens lineage formation.

Keywords: Differential mRNA Expression

overall_design: Three biological replicate experiments were performed with HSF null and wildtype lenses.

first: Louise

last: Wolf

first: Ales

last: Cvekl

last: Zavadil

first: Akira

last: Nakai


title: Deficient of IL-18 in mice leads to the reduction of neuropeptides in the amygdala related with behavioral change

city: Tokushima

first: Yuta

address: 3-18-15 Kuramoto-cho

department: Stress Science

institute: Institue for Health Biosciences, The University of Tokushima Graduate School

summary: Interleukin (IL)-18 is recognized as a multifunctional mediator in inflammation and immune responses. In addition, the production of IL-18 is stimulated by physiological and/or psychological stress implicated in several behavioral disorders. However, it still remains unclear about the role of IL-18 on the central nervous system. In this study, we analyzed gene expression of 6 brain regions; the olfactory bulb, prefrontal cortex, striatum, amygdala, hypothalamus, and hippocampus. Microarray analysis indicated the regional differences of expression in IL-18-/- mice. In particular, the most profound change was observed in the amygdala, in which 1,237 genes were differentially expressed.

overall_design: We purchased IL-18-/- mice and C57BL/6 mice from Charles River Japan . To produce F1 generation mice, three male IL-18-/- mice were mated with six female C57BL/6J mice. We mated F1 mice and created their F2 littermates. Six week-old F2 mice littermates were weaned. At 12 weeks, mice were sacrificed at 14:00 under general anesthesia with diethyl ether. After the systemic perfusion with cold phosphate-buffered saline through the heart using a syringe attached to a 21-G needle, the whole mouse brains were removed. Coronal brain sections (1 mm thick) were prepared on ice using a brain slicer . The olfactory bulb was sliced between 3.5 and 4.5 anterior to bregma. The prefrontal cortex was sliced between 2.5 and 3.5 mm anterior to bregma. The striatum was sliced between -0.5 and 0.5 mm posterior to bregma. The hypothalamus, the amygdala, and the hippocampus were sliced between 1.5 and 2.5 mm posterior to bregma. Total RNA was immediately prepared from these samples using TRIzol  and purified by RNeasy kit.

first: Toshihito

last: Tanahashi

first: Sakurako

last: Katsuura

first: Ken

last: Kurokawa

first: Kensei

last: Nishida

first: Yuki

last: Kuwano

first: Tomoko

last: Kawai

first: Shigetada

last: Teshima-Kondo

first: Hiroyoshi

last: Sei

first: Kazuhito

last: Rokutan


title: Sex-related differences in gene expression following Coxiella burnetii infection: potential role of circadian rhythm

status: Public on Oct 02 2010

city: Lyon

first: Julien

last: Textoris

address: Hôpital Edouard herriot - Pavillon P; 5 place d'Arsonval

department: Medical Diagnostic Discovery Department (MD3)

institute: bioMérieux

summary: Q fever, a zoonosis due to Coxiella burnetii infection, exhibits sexual dimorphism; men are affected more frequently and severely than women for a given exposure. Here we explore whether the severity of C. burnetii infection in mice is related to differences in male and female gene expression profiles. Mice were infected with C. burnetii for 24 hours, and gene expression was measured in liver cells using microarrays. Multiclass analysis identified 2,777 probes for which expression was specifically modulated by C. burnetti infection. Only 14% of the modulated genes were sex-independent, and the remaining 86% were differentially expressed in males and females. Castration of males and females showed that sex hormones were responsible for more than 60% of the observed gene modulation, and this reduction was most pronounced in males.  Using functional annotation of modulated genes, we identified four clusters enriched in males that were related to cell-cell adhesion, signal transduction, defensins and cytokine/Jak-Stat pathways. Up-regulation of the IL-10 and Stat-3 genes may account for the high susceptibility of men with Q fever to C. burnetii infection and autoantibody production. Two clusters were identified in females, including the circadian rhythm pathway, which consists of positive (Clock, Arntl) and negative (Per) limbs of a feedback loop. We found that Clock and Arntl were down-modulated whereas Per was up-regulated; these changes may be associated with efficient bacterial elimination in females but not in males, in which an exacerbated host response would be prominent. This large-scale study revealed for the first time that circadian rhythm plays a major role in the anti-infectious response of mice, and it provides a new basis for elucidating the role of sexual dimorphism in human infections.

overall_design: Liver transcriptome was analyzed using whole genome microarray. Forty mice were divided into 8 groups of five mice upon three binary factors: sex, infection and castration. Four Samples were excluded from final analysis (see Data Processing for additional details).

first: Leang

middle: H

last: Ban

first: Christian

last: Capo

first: Didier

last: Raoult

first: Marc

last: Leone

last: Mege


title: Murine Prostate Tissue: Rb1 null vs. Rb1 E2F binding deficient mutant

city: Buffalo

first: David

last: Goodrich

state: NY

address: Elm and Carlton

department: Pharmacology&Therapeutics

institute: Roswell Park Cancer Institute

summary:
Transcriptional profilling of 60 day old prostate tissue from Rb1F/F:Trp53F/F:PB-Cre4 or Rb1R654W/F:Trp53F/F:PB-cre4 mice versus wild type prostate tissue.
Profiles used to compare deregulation of known E2F target genes in prostate tissue expressing a mutant Rb1 gene to tissue lacking Rb1 expression.

overall_design: Tissue from two Rb1F/F:Trp53F/F:PB-Cre4 (null) mice or two Rb1654/F:Trp53F/F:PB-cre4 (mutant) mice compared to a pool of tissue from 3 wild type mice using two color arrays.

first: Yangqing

last: Wang


title: Stage-specific sensitivity to p53 restoration in lung cancer: tumor data

first: Charles

last: Whittaker

overall_design: 18 tumors of different grade and treatment status. 6 treated grade 3, 4 treated grade2, 4 untreated grade3, 4 untreated grade2

last: Feldser

first: Kamena

last: Kostova

first: Monte

last: Winslow

first: Sarah

last: Taylor

first: Chris

last: Cashman

first: Francisco

last: Sanchez-Rivera

first: Rebecca

last: Resnick

first: Roderick

last: Bronson

first: Michael

last: Hemann

first: Tyler

last: Jacks


title: Liver gene expression analysis of male and female C57BL/6 mice treated with glucocorticoid.

city: RTP

first: NIEHS

last: Microarray Core

state: NC

address: 111 T.W. Alexander Drive

department: DIR

institute: NIEHS

summary: Glucocorticoids are widely used therapeutically to suppress inflammatory/immune responses and most of their effects are produced either by altering transcription of specific genes directly, or by altering the expression of transcription factors that subsequently alter the expression of downstream genes. Relevant data from previous studies indicate that the number of genes regulated by glucocorticoid receptor exceeds 4000 in cells and that 358 different genes are regulated in the liver of adrenalectomized males rats treated with a chronic infusion of methylprednisolone for up to 1 week . However, differences in gene expression between males and females in response to glucocorticoid treatment in a mouse model are not known.

overall_design: The animals (males and females adrenalectomized C57Bl/6 mice) were treated with vehicle or dexamethasone 1mg/Kg (i.p.) and 6 hours later the liver will be harvested to RNA extraction using the Qiagen RNEASY midi kit . The study was performed with 3 biological replicates: 3 control males; 3 control females, 3 dexamethasone treated males and 3 dexamethasone treated females.

first: Danielle

last: Duma

first: Kevin

last: Gerrish


title: Gene expression analysis of IL-4 primed bone marrow macrophages isolated from Irf4-deficient or heterozygous mice

status: Public on Oct 01 2010

city: Regensburg

last: Rehli

address: F.-J.-Strauss-Allee 11

department: Internal Med III

institute: University Hospital Regensburg

summary:
To analyse the Irf4-dependent transcriptional changes of mouse bone marrow-derived macrophages (BMM) in response to IL-4, we have employed whole genome microarray expression profiling. For this purpose, bone marrow cells were isolated from 8 to 12 weeks old Irf4-deficient or heterozygous mice and cultured in the presence of the macrophage colony-stimulating factor (M-CSF) . After seven days of culture, IL-4 was added for 4 and 18 hours.

Keywords: Mouse strain comparision; Gene expression profiling

overall_design: IL-4 induced gene expression was investigated in mouse bone marrow-derived macrophages (BMM) of Irf4-deficient or heterozygous mice. BMM were incubated with mouse recombinant IL-4  for 4 or 18 hours or without for 18 hours. Three independent experiments were performed at each time point (mock, 4 and 18 hours) using littermates for each experiment.

first: Carol

last: Chartouni


title: Transcriptomic definition of curcumin treated microglia

status: Public on Sep 29 2010

first: Thomas

last: Langmann

address: Franz-Josef-Strauss-Allee 11

department: University of Regensburg

institute: Institute of Human Genetics

summary: Curcumin is a potent modulator of the inflammatory transcriptome in microglia

overall_design: We have performed global gene expression analysis of BV-2 microglial cells under the following conditions: untreated, 20 µM Curcumin-treated, 100ng/ml LPS-treated, or 20 µM Curcumin-treated + 100ng/ml LPS-treated


title: Potential mechanisms of endocrine disruptors as revealed by uterine gene profile

status: Public on Oct 07 2010

summary: Females were ovariectomized and injected with sesame oil, estradiol in sesame oil, BPA in sesame oil or HPTE in sesame oil. Uterine tissue was collected after 2 or 24 hours. RNA was analyzed by microarray compare ealry and late responses to a potent and a weak estrogen agaonist.

overall_design: 3 uteri per group were analyzed individually on one-color Agilent arrays (note: estradiol treatment at 24 hr only has 2 replicates).

first: Sylvia

middle: C

last: Hewitt

first: Kenneth

last: Korach


title: Expression data from mouse  T-cell lymphomas

status: Public on Oct 19 2010

city: New York

first: Adolfo

middle: A

last: Ferrando

address: 1130 St Nicholas Ave Irving Cancer Research Center 5-505A

department: Institute for Cancer Genetics

institute: Columbia University

summary:
Transgenic expression of  TLX1 induces T-cell leukemias in mice.
We used microarrays to identify the gene expression signatures associated with TLX1 tumors compared with different genetic models T acute lymphoblastic lymphoma.

overall_design: RNA extraction from T-cell tumors from mice with different T-cell lymphoma-predisposing genetic backgrouds.

first: Maria

last: Sulis


title: Differential expression of genes in liver of mice with a nonfunctional helicase domain of the Wrn protein treated with resveratrol compared to untreated wild type mice.

city: Lausanne

first: Eric

last: Paquet

state: Vaud

address: Station 15  CH - 1015

department: Life sciences

country: Switzerland

institute: EPFL

summary: Werner syndrome (WS) is a rare disorder characterized by the premature onset of a number of age-related diseases. The gene responsible for WS is believed to be involved in different aspects of transcription, replication, and/or DNA repair. We generated a mouse model with a deletion in the helicase domain of the murine WRN homologue that recapitulates most of the WS phenotypes including an abnormal hyaluronic acid excretion, higher reactive oxygen species (ROS) levels, increased genomic instability and cancer incidence resulting in a 10-15% decreased life span expectancy. In addition, WS patients and Wrn mutant mice show hallmarks of a metabolic syndrome including premature visceral obesity, hypertriglyceridemia, insulin-resistant diabetes type 2 and associated cardiovascular diseases. In this study, we compared the expression profile of liver tissues from 9 months old Wrn mutant treated with a standard diet supplemented with 0.04% resveratrol and wild type animals fed with standard diet only. Resveratrol is a calorie restriction mimetic. Gene set enrichment analysis of the microarray data indicated that reseveratrol-treated Wrn mutant mice exhibited down-regulation of genes normally decreased in several transgenic mouse models of hepatoma. In addition, resvratrol-treated Wrn mutant mice also exhibited a decrease in the expression of genes involved fatty acid metabolism and PPAR signaling pathways. Resvratrol-treated Wrn mutant mice also increased the expression of genes involved in steroid and cholesterol biosynthesis, xenobiotic metabolisms as well as inflammation. Finally, resveratrol improved insulin-resistance and the hyperglycemia but had no impact on dyslipidemia and mean life span of Wrn mutant mice.

overall_design: Microarray analyses were performed on the liver tissues of 9 months old mice. Four independent biological replicates of this experiment (wild type vs resveratrol treated Wrn helicase mutant mice) were carried out with a dye swap on two replicates of each genotype.

first: Adam

last: Labbé

first: Chantal

last: Garand

first: Victoria

last: Cogger

first: David

middle: G

last: Le Couteur

first: Michel

last: Lebel


title: Reprogramming of fibroblasts into induced pluripotent stem cells with Bmi1

status: Public on Sep 18 2010

city: Seoul

first: Seungkwon

last: You

address: Anam-dong Sungbuk-go

country: South Korea

institute: Korea University

summary: Somatic cells can be reprogrammed into induced pluripotent stem (iPS) cells by Oct4, Sox2, Klf4, plus c-Myc. Recently, Sox2 plus Oct4 were shown to reprogram fibroblasts and Oct4 alone to reprogram mouse and human neural stem cells (NSCs) into iPS cells. Here we report that Bmi1 leads to dedifferentiation of mouse fibroblasts into NSC-like cells and, in combination with Oct4, replaces Sox2, Klf4 and c-Myc during reprogramming fibroblasts to iPS cells. Furthermore, activation of sonic hedgehog signalling (by Shh, purmorphamine, or oxysterol) replaces the effects of Bmi1, and, in combination with Oct4, reprograms mouse embryonic and adult fibroblasts into iPS cells. One-and two-factor iPS cells are similar to mouse embryonic and adult fibroblasts into iPS cells in global gene expression profile, epigenetic status, in vitro and in bibo differentiation into all three ferm layers, as well as teratoma formation and germline transmission in vivo. These data support that fibroblasts can be reprogrammed into iPS cells by Oct4 alone.

overall_design: Total RNAs were isolated from indicated cells and labeled with Cy3. Hybridization was performed once for each sample.


title: Wild-type bone-marrow derived macrophages response to Escherichia coli lipopolysaccharide (LPS)

first: Benoit

last: Desnues

summary: We have employed whole genome microarray expression profiling to identify differently expressed genes following stimulation of wild-type bone-marrow derived macrophages with Escherichia coli lipopolysaccharide (LPS). Macrophages were stimulated with LPS (100 ng/ml) for 6 hours and a signature was identified that distinguished between infected and control samples. Expression of several genes from this signature was quantified in the same RNA samples by real-time PCR, confirming the predicted macrophage response pattern.

first: Jean-Louis

last: Mège


title: The role of microRNAs in hepatic thyroid hormone signalling

status: Public on Aug 20 2010

city: ottawa

first: hongyan

last: dong

address: 50 colombine Dr.

institute: health canada

type:
Expression profiling by array
Other

summary: MicroRNAs (miRNAs) are extensively in diverse biological processes. However, very little is known about the role of miRNAs in mediating thyroid hormones (TH) action. Maintenance of appropriate TH levels is known to be critically important for development, differentiation and maintenance of metabolic balance in mammals. We induced transient hypothyroidism in juvenile mice by short term exposure to methimazole and perchlorate from post natal day (PND) 12 to 15. The expression of miRNAs in the liver was analyzed with the Taqman Low Density Array (containing up to 600 rodent microRNAs). We found the expression of 40 miRNAs was significantly altered in the liver of hypothyroid mice compared to euthyroid controls. Among the miRNAs, miR-1/206/133 exhibited a massive increase in expression (50 – 500 folds). To further explore TH effect on miR-1/206/133, we treated mouse hepatocyte AML 12 cells with 10 nm T3 for 1 hr and 24 hrs. TH treatment induced the down-regulation of miR-1/206/133b at both time points, reaching statistical significance at 24 hrs.  To identify the genes targeted by these miRNAs, DNA microarrays were used to examine hepatic mRNA levels in the hypothyroid mouse model alongside controls. We found transcripts from 92 known genes were significantly altered in hypothyroid mice. Web-based target predication softwares (TargetScan and Microcosm) identified 14 of these transcripts as targets of miR-1/106/133. The vast majority of these mRNA targets were significantly down-regulated in hypothyroid mice, corresponding well with the up-regulation of miR-1/206/133 in hypothyroid mouse liver. The results suggest that TH regulation of these genes may occur secondarily via the reduced repression consequent to TH-induced down-regulation of miR-1/206/133. These studies provide novel insight into the role of miRNAs in mediating TH regulation of gene expression.

platform_organism:
Mus musculus
Rattus norvegicus

overall_design: Agilent two-color microarray were used to perform gene expression profile in euthyroid and hypothyroid male mouse livers, 5 biological replicates.  TLDA (Taqman microRNA Array) was used to explore the miRNA expression profile in euthyroid and hypothyroid male mouse livers, 4 biological replicates.

first: Hongyan

last: Dong

first: Martin

last: Paquette

first: Andrew

last: Williams

first: R

last: Zoeller

first: Mike

last: Wade

first: Carole

last: Yauk


title: Aldosterone-Regulated Expression Data in Mouse Aorta

status: Public on Aug 12 2010

city: Boston

first: Lakshmanan

last: Iyer

address: 136 Harrison Ave

department: Neuroscience

institute: Tufts University

summary:
The steroid hormone aldosterone plays a role in vascular function and disease. Aldosterone activates the mineralocorticoid receptor (MR), a ligand-activated transcription factor. MR have been found to be expressed in vascular cells and vessels.
We used microarrays to identify the global programme of gene expression changes in mouse aortas treated with vehicle (DMSO) or aldosterone.

overall_design: Wild type C57Bl6 male mice were treated with spironolactone (20 mg/kg/day, an MR antagonist) for 5 days by Sub-cutaneous pellet to suppress basal MR-mediated gene expression. Aortas were then harvested and treated ex vivo in organ culture with vehicle or 100 nM aldosterone for 2, 4, or 8 hours. Three aortas were pooled for each timepoint and treatment, and three pooled biological replicates were performed.

first: Iris

middle: Z

last: Jaffe


title: Gene expression profile of bone marrow with post-irradiation radioprotector

status: Public on Sep 27 2010

city: Chiba

first: Kaori

last: Imadome

state: Chiba

address: Anagawa 4-9-1

department: Research Center of Charged Particle Therapy

institute: National institute of radiological sciences

summary:
To elucidate the mechanism of the in vivo radioprotection activity of Zn-containing heat-treated Saccharomyces cerevisiae yeast (Zn-yeast), expression changes in bone marrow after whole body irradiation (WBI) with concomitant treatment of Zn-yeast were analyzed using microarray technology.

Keywords: mouse, bone marrow, Zn-containing heat-treated yeast administration, gamma-irradiation

overall_design: Zn-yeast suspension was administered i.p. into C3H mice immediately after 7.5 Gy WBI. Bone marrow from irradiated mice was extracted at 6 hours after irradiation and analyzed by microarray containing of 44,000 probes.

first: Mayumi

last: Iwakawa


title: Mouse embryonic kidneys (E13.5): HDAC inhibitor (HDACi) treated vs. Control

status: Public on Aug 01 2010

city: New Orleans

first: Samir

middle: S

last: El-Dahr

address: 1430 Tulane Ave

department: Pediatrics

institute: Tulane University School of Medicine

summary: Transcriptional profiling of cultured CD1 mouse embryonic kidneys (E13.5) comparing  HDACi-treated kidneys with control drug-treated kidneys. Studies in our lab showed that pharmacological inhibition of HDAC activity in ex-vivo cultured metanephroi results in extensive defects in kidney development, including impaired UB branching, tubulogenesis, and glomerulogenesis, accompanied by cell cycle arrest and apoptosis.The goal of the microarray analysis was to elucidate the morphogenetic pathways affected by HDACi.

overall_design: Two-condition experiment, HDACi-treated E13.5 kidneys (Scriptaid 2.0 μg/ml x 6hrs) vs. Control drug-treated E13.5 kidneys (Nullscript 2.0 μg/ml x 6hrs). Biological replicates: 3 control replicates, 3 HDACi-treated replicates. Two-color Agilent 4x44k chips with dye-swap on 2 of 4 arrays.

first: Shaowei

last: Chen

first: Dimcho

last: Bachvarov


title: Profiling of cutaneous tumors

status: Public on Jul 07 2010

city: lille

first: frédéric

last: leprêtre

address: Boulevard du Pr Leclercq

department: CHU of Lille, CBP

institute: Lille University

summary: Metastasis and drug-resistance are major problems in cancer chemotherapy. The purpose of this work was to analyze the molecular mechanisms underlying the invasive potential of drug-resistant colon carcinoma cells. Cellular models included the parental HT-29 cell line and its drug-resistant derivatives selected after chronic treatment with either 5-fluorouracil (5-FU), methotrexate (MTX), doxorubicin (DOX) or oxaliplatin (OXA). Drug-resistant invasive cells were compared to non invasive cells using cDNA microarray, qRT-PCR, flow cytometry, immunoblots and ELISA. Functional and cellular signaling analyses were undertaken using pharmacological inhibitors, function-blocking antibodies, and silencing by retrovirus-mediated RNA interference. 5-FU- and MTX-resistant HT-29 cells expressing an invasive phenotype in collagen type I and a metastatic behaviour in immunodeficient mice exhibited high expression of the chemokine receptor CXCR4. Macrophage migration inhibitory factor (MIF) was identified as the critical autocrine CXCR4 ligand promoting invasion in drug-resistant colon carcinoma HT-29 cells. Silencing of CXCR4 and impairing the MIF-CXCR4 signaling pathways by ISO-1, pAb FL-115, AMD-3100, mAb 12G5, and BIM-46187 abolished this aggressive phenotype. Induction of CXCR4 is associated with up-regulation of two genes encoding transcription factors previously shown to control CXCR4 expression (HIF-2a and ASCL2) and maintenance of intestinal stem cells (ASCL2). Enhanced CXCR4 expression was detected in liver metastases resected from colon cancer patients treated by the standard FOLFOX regimen. Combination therapies targeting the CXCR4-MIF axis can potentially counteract the emergence of the invasive metastatic behaviour in clonal derivatives of drug-resistant colon cancer cells.

platform_organism:
Homo sapiens
Mus musculus

overall_design:
Samples:
HT-29 cell clones were obtained by limiting dilution from HT-29 subpopulations resistant to methothrexate (HT-29 5M21 cell clone) and or to 5-Fluoro-uracil (HT-29 5F7 and HT-29 5F31). Samples were provided by Dr. T Lesuffleur.

Xenografts:
HT-29 5M21, HT-29 5F7, and HT-29 5F31 xenografts were obtained by a first subcutaneous inoculation of cells in Nude mice and then fragments of subcutaneous tumors were reimplantated in SCID mice.

First experiment of microarrays: HT-29 5M21 and HT-29 5F7 cells (that are invasive in in vitro assays on type I collagen) were compared to HT-29 5F31 cells (that are not invasive in vitro on type I collagen). Samples were co-hybridized on Agilent Human 44K GEP arrays (respectively 5F31 vs 5M21, 5F31 vs 5F7, 5M21 vs 5F31 and 5F7 vs 5F31).

Second experiment of microarrays: HT-29 5M21 and HT-29 5F7 xenografts (that develop metastases in immuno-deficient mice lungs) were compared to HT-29 5F31 xenografts (that do not develop metastases in immuno-deficient mice lungs). Samples were consequently co-hybridized on human and mouse 4x44K GEP arrays (respectively AG41_5F31-5M21-138869, AG39_5F31-5F7-138867, AG42_5M21-5F31-138870 and AG40_5F7-5F31-138868 for human microarrays; 5M21_5F31_27033_4, 5F31_5M21_27033_3, 5F7_5F31_27033_2 and 5F31_5F7_27033_1_1 for mouse microarrays).

first: Guillemette

last: Huet


title: Nuclear orphan receptor TAK1/TR4-deficient mice are protected against obesity-linked inflammation, hepatic steatosis, and insulin resistance

first: NIEHS

last: Microarray Core

summary: The nuclear receptor TAK1/TR4/NR2C2 is expressed in several tissues that are important in the control of energy homeostasis. TAK1-deficient (TAK1-/-) mice are resistant to the development of age- and high fat diet (HFD)-induced metabolic syndrome. Biochemical analysis showed significantly lower hepatic triglyceride levels and reduced lipid accumulation in adipose tissue in TAK1-/- mice compared to wild type (WT) mice. Gene expression profiling analysis revealed that the expression of several genes encoding proteins involved in lipid uptake and triglyceride synthesis and storage, including Cidea, Cidec, Mogat1, and CD36, was greatly decreased in the liver of TAK1-/- mice. Moreover, TAK1-/- mice exhibit reduced infiltration of inflammatory cells and expression of inflammatory genes in adipose tissue and were resistant to the development of glucose intolerance and insulin resistance. TAK1-/- mice consume more oxygen and produce more carbon dioxide than WT mice suggesting a higher rate of energy expenditure. Together, these results indicate that TAK1 plays a critical role in the regulation of energy and lipid homeostasis and potentiates the development of metabolic syndrome. Our study suggests that TAK1 might provide a novel therapeutic target in the management of metabolic syndrome.

overall_design: For microarray liver total RNAs were purified from WT and TAK1 KO mice and applied on Agilent mouse genome chip. Liver from 1 year old- WT and TAK1 KO mice.

first: H

last: Kang

first: K

last: Okamoto

first: Y

last: Kim

first: A

last: Jetten


title: Expression data from ETO2/LMO2 knockdown G1E-ER-GATA-1 cells

status: Public on Sep 25 2010

first: Tohru

last: Fujiwara

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

department: Hematology and Rheumatology

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

overall_design: Refer to individual Series


title: Expression data from LMO2 knockdown G1E-ER-GATA-1 cells

summary: We used microarrays to examine what genes could be regurated by LMO2 in erythroid cells.

overall_design: Comparing expression profile in murine G1E-ER-GATA-1 cells treated with control and Lmo2 siRNA on Agilent array.  After siRNA transfection, the cells were treated with b-estradiol for 24h to induce GATA-1-mediated erythroid maturation.

first: Hsiang-Ying

last: Lee

first: Rajendran

last: Sanalkumar

first: Emery

last: Bresnick


title: Effect of Malat1 ASO on Neuro2 neuroblastoma cells transcriptome

status: Public on Jul 26 2010

city: Paris

first: Laurent

last: Jourdren

address: 46 rue d'Ulm

department: Biologie

institute: École Normale Supérieure

summary:
We investigated the effects of transfecting Malat1 antisense oligonucleotides on the whole Neuro2 neuroblastoma transcriptome. In this work, global transcription analyses were combined with detailed analyses of some synaptic genes. Our results provide insight on Malat1 effect on the regulation of gene expression in a mouse neuroblastoma cell line.

Keywords: Comparative transcriptome analysis from Mus Musculus Neuro2 neuroblastoma cells transfected by Malat1 or Scamble oligodeoxynucleotides.

overall_design: Three biological samples in dye swap

first: Delphine

last: Bernard

first: Kannanganattu

last: V. Prasanth

first: Sabrina

last: Colasse

first: Tetsuya

last: Nakamura

first: Zhenyu

last: Xuan

first: Michael

last: Q. Zhang

first: Fanny

last: Coulpier

first: Antoine

last: Triller

first: David

last: L. Spector

first: Alain

last: Bessis


title: Comparison of murine colonic mucosal DNA between postnatal day 90 C57BL/6 wild type (WT) and their toll-like receptor 2 knockout (Tlr2-/-) counterparts by methylation specific amplification microarray (MSAM), and whole genomic gene expression profiling

status: Public on Jul 01 2010

city: Houston

first: Richard

last: Kellermayer

address: One Baylor Plaza

institute: Baylor College of Medicine

type:
Methylation profiling by array
Expression profiling by array

summary:
BACKGROUND & AIMS: Toll-like receptor 2 (Tlr2) is important in bacterial pattern recognition and has been recognized as a modifier of intestinal inflammation. In this study we sought to determine the epigenomic, transcriptomic and microbiomic consequences of Tlr2 deficiency in the colonic mucosa of mice to gain insights into biological pathways that shape the interface between the gut microflora and the mammalian host.
METHODS: Colonic mucosa from C57BL/6 and Tlr2-/- mice was interrogated by methylation specific amplification microarray (MSAM) to screen for changes in DNA methylation, with bisulfite pyrosequencing validation. Transcriptomic changes in the same tissue were analyzed by microarray expression profiling and real time RT-PCR. The mucosal microbiome was studied by high throughput, detailed pyrosequencing of 16S RNA.
RESULTS: Tlr2 deficiency influenced the methylation of about 1% of the interrogated genome and resulted in a significant expression change in a similar percentage of all transcripts studied. Importantly, gene ontology analysis revealed that the expression of genes involved in immune processes is significantly modified by the absence of Tlr2, some of which have been already linked to inflammatory bowel diseases (Stat1, Anpep), for example. Overlaps between DNA methylation and gene expression changes were confirmed at Anpep and Ifit2. The epigenomic and transcriptomic modifications associated with alteration in mucosal microbial composition, affecting 11% of the detected bacterial species in the Tlr2-/- animals.
CONCLUSIONS: Tlr2 deficiency induces colonic mucosal epigenomic, transcriptomic and microbiomic changes underscoring the intricate network of biological processes that provide the link between genotype and phenotype in mammals. Our findings bare implications for common gastrointestinal disorders such as IBD and colon cancer.

overall_design:
[MSAM]: Methylation profiling. Two independent Tlr2-/- to WT comparisons were performed as follows. Samples were labelled with Cy3 (WT) and Cy5 (Tlr2-/-) and two independent  Tlr2-/- to WT comparisons were done on a 2x105k microarray containing probes, covering 33,404 (81% of all) SmaI intervals between 100 bp and 2.2 kb in the mouse genome.

[mRNA]: mRNA profiling.  4 independent Tlr2-/- to WT comparisons were performed as follows. RNA (0.4ug) samples were processed and labelled with Cy3 and Cy5 (Quick Amp labelling kit, two color, Agilent technologies)  and 4 independent Tlr2-/- to WT comparisons were done on Agilent technologies 4x44k whole genomic expression microarray G2519F, Amadid:014868).

The Supplementary files below contain processed data from the MSAM and expression microarrays.
For the MSAM: an interval was considered a 'hit' if the averaged probe ratios within an interval showed a >1.6 fold change in both Tlr2-/- vs. WT comparisons.
For the expression microarrays: transcripts were considered a 'hit' if probe average intensities showed a >1.6 fold change in at least two microarray comparisons out of four, with the remaining arrays not contradicting the increase or decrease of expression (i.e.: 1 or above 1 in case at least two other >1.6; 1 or less than 1 in case at least two other <0.625).


title: Impact of MAA on mouse Leydig cell gene expression (Mus musculus)

status: Public on Jul 06 2010

middle: J.

last: Waxman

address: 5 Cummington Mall

department: Department of Biology and Bioinformatics Program

institute: Boston University

summary: Methoxyacetic acid (MAA) is the active metabolite of the widely used industrial chemical ethylene glycol monomethyl ether, an established testicular toxicant.  MAA induces the degradation of testicular germ cells in association with changes in gene expression in both germ cells and Sertoli cells of the testis.  This study investigates the impact of MAA on gene expression in testicular Leydig cells, which play a critical role in germ cell survival and male reproductive function.  Cultured mouse TM3 Leydig cells were treated with MAA for 3, 8, and 24 h and global gene expression was monitored by microarray analysis.  A total of 3,912 MAA-responsive genes were identified.  Ingenuity Pathway analysis identified reproductive system disease, inflammatory disease and connective tissue disorder as the top biological functions affected by MAA.  The MAA-responsive genes were classified into 1,366 early responders, 1,387 mid-responders, and 1,138 late responders, based on the time required for MAA to elicit a response.  Analysis of enriched functional clusters for each subgroup identified 106 MAA early response genes involved in transcription regulation, including 32 genes associated with developmental processes and 60 DNA-binding proteins that responded to MAA rapidly but transiently, and which may contribute to the downstream effects of MAA seen for large numbers of mid and late response genes.  Genes within the phosphatidylinositol/phospholipase C/calcium signaling pathway, whose activity is required for potentiation of nuclear receptor signaling by MAA, were also enriched in the set of early MAA response genes.  These findings on the progressive changes in gene expression induced by MAA in Leydig cells may help elucidate the signaling pathways perturbed by this testicular toxicant and explain its mechanism of toxicity at the gene level.

overall_design: Mouse TM3 Leydig cells (American Type Culture Collection, Manassas, VA) were grown in DMEM-F12 medium containing 5% horse serum and 2.5% FBS.  Cells were grown to ~60% confluence and treated with culture medium alone, or with culture medium containing 1 mM or 5 mM MAA for either 3, 8 or 24 h.  Total RNA was then isolated using TRIzol reagent, followed by incubation with RQ1 RNAse-free DNAse for 1 h at 37°C and then heating at 75°C for 5 min using the manufacturer’s protocol.  A total of 6 cultures of TM3 cells were independently treated with MAA under each of the 6 treatment conditions specified above (i.e., 1 mM or 5 mM MAA for either 3, 8 or 24 h), and the corresponding 6 sets of RNA samples were validated by RNA integrity analysis (Agilent Bioanalyzer).  Each RNA sample was also validated by qPCR analysis using SYBR Green I-based chemistry and primers specific for 3 genes known to respond to MAA (Cyp17a1, Shbg, and Igfbp3) to verify consistency of the MAA responses.  The 6 RNA samples were then used to prepare two independent pools (n=3 RNA samples each) for microarray analysis with dye swaps. Sample labeling, hybridization to microarrays, scanning and calculation of normalized expression ratios were carried out at the Wayne State University Institute of Environmental Health Sciences microarray facility using Alexa 555 and Alexa 647 aminoallyl-aRNA samples

first: Gargi

last: Bagchi

first: Yijing

last: Zhang

middle: J


title: Expressoin data from iPSC with different cell of origin

status: Public on Jul 20 2010

first: Jose

middle: Maria

last: Polo

address: 85 Cambridge Street, CPZN 4200

department: Cancer Center

institute: MGH

summary:
Induced pluripotent stem cells (iPSCs) have been derived from various somatic cell populations through ectopic expression of defined factors. It remains unclear whether iPSCs generated from different cell types are molecularly and functionally similar.
We use expresson profiling to determine differnces in iPSCs with different cell of origin.

overall_design: Using a secondary system, we derived iPSCs from tail tip-derived fibroblasts (TTF-iPSC), splenic B cells (B-iPSC), bone marrow-derived granulocytes (Gra-iPSC) , skeletal muscle precursors (SMP-iPSC) and T cells (T-iPSC).

first: Konrad

last: Hochedlinger


title: Murine bone marrow immature B cells: autoreactive versus non-autoreactive

status: Public on Aug 31 2010

city: Denver

first: Roberta

last: Pelanda

state: CO

address: 1400 Jackson Street

department: Immunology

institute: National Jewish Health

summary: Transcriptional profiling of mouse bone marrow B220+CD23–CD43–IgD– autoreactive immature B cells from 3-83Igi,Rag1-/-,H-2b mice relative to non-autoreactive immature B cells from 3-83Igi,H-2d mice. Goal was to determine genes that potentially mediate negative and positive selection of immature B cells.

overall_design: Biological replicates: 2 autoreactive replicate against, 2 non-autoreactive replicates


title: Expression data from ETO2 knockdown G1E-ER-GATA-1 cells

city: Sendai

first: Tohru

last: Fujiwara

institute: Tohoku University Graduate School of Medicine

summary: We used microarrays to examine what genes could be regulated by ETO2 in erythroid cells.

overall_design: Comparing expression profile in murine G1E-ER-GATA-1 cells treated with control and ETO2(Cbfa2t3) siRNA on Agilent array. After siRNA transfection, the cells were treated with b-estradiol for 24h to induce GATA-1-mediated erythroid maturation.

first: Hsiang-Ying

last: Lee

first: Rajendran

last: Sanalkumar

first: Emery

last: Bresnick


title: Gene expression profile associated with the PDZ ligand-motif of HPV16-E6 oncoprotin in the skin of transgenic mice models

status: Public on Jul 27 2010

city: Mexico City

first: Laura

middle: I

last: Uribe

state: DF

address: Periferico Sur 4124 Col. Ex rancho de Anzaldo

department: Research

country: Mexico

institute: INMEGEN

summary:
The K14E6 transgenic mice developskin hyperplasia,benign tumors and skin cancer. The tumor formation capacity diminishes when E6 lacks its PDZ ligand-motif.
This study aims to compare the transciptional profiles of transgenic K14E6 mice with K14E6 Δ146-151 (lacking the PDZ domain) in order to explore the role of PDZ in early skin carcinogenesis.

overall_design: Skin tissue from three different strains of mice were dissected for RNA extraction, processing and hybridization in Affymetrix Mouse Genome 430 2,0 array. We processed three biological replicates per strain. 3 mice were used for each replicate pool for a final RNA concentration of 3 micrograms. The arrays were analyzed using Partek Genomics suite software.

first: Alejandra

last: Roman-Rosales

first: José

last: Bonilla-Delgado

first: Enrique

last: Garcia-Villa

last: Uribe-Figueroa

first: Claudia

last: Rangel-Escareno

first: Alfredo

last: Hidalgo-Miranda

first: Paul

middle: F

last: Lambert

first: Patricio

last: Gariglio


title: Estrogen response uterine gene profile in Ex3αERKO

status: Public on Jul 23 2010

first: NIEHS

last: Microarray Core

address: 111 T.W. Alexander Drive

institute: NIEHS

summary: WT and Ex3aERKO females were ovariectomized and injected with saline or estradiol. Uterine tissue was collected after 2 or 24 hours. RNA was analyzed by microarray to determine if the Ex3aERKO mice would lack the residual transcritpional resposnes seen in the previous aERKO model.

overall_design: 3 uteri per group were analyzed individually on one-color Agilent arrays. Comparisons were made within ERa genotype (WT saline to WT E treated; Ex3aERKO saline to Ex3aERKO E treated)

first: Sylvia

last: Hewitt

first: Grace

middle: E

last: Kissling

first: Karen

last: Fieselamsn

first: Friederike

middle: L

last: Jayes

first: Kevin

last: Gerrish

first: Kenneth

last: Korach


title: Fgf8 E18.5 hypomorph versus control mouse fetal lungs

status: Public on Sep 20 2010

city: Salt Lake City

first: Anne

last: Moon

state: UT

department: Eccles Institute of Human Genetics

institute: University of Utah

summary: We set out to look for genome wide gene expression changes due to deficiency of Fgf8 in the lung.

overall_design: RNA from 3 lungs from each genotype  (mutant and littermate wild type control) are pooled for each cDNA synthesis and hybridized to individual array for a quadruple biologic repeat of the  experiment


title: Control of Embryonic Stem Cell State by Mediator and Cohesin (Agilent gene expression data)

city: Cambridge

first: Richard

last: Young

address: 9 Cambridge Center

institute: Whitehead Institute for Biomedical Research

summary: The key transcription factors that control the embryonic stem cell gene expression program have been identified, but how they function to implement this program is not well understood.  While screening for genes essential for maintenance of ES cell state, we identified many components of the Mediator and Cohesin complexes.  Mediator and Cohesin were found to physically and functionally connect the enhancers and core promoters of active genes.  An ES cell Mediator complex was found to copurify with Cohesin and its loading factor Nipbl, and normal levels of these proteins were essential for expression of the genes they occupy and for maintenance of ES cell state.

overall_design: See associated publication.

first: Michael

last: Kagey

first: Steve

last: Bilodeau

first: Jamie

last: Newman

first: David

last: Orlando


title: Dnmt3a-dependent non-promoter DNA methylation facilitates transcription of neurogenic genes

status: Public on Jun 25 2010

city: Los Angeles

first: Yi

last: Sun

state: CA

address: 635, Charles E. Young Dr. South

department: Molecular and Medical Pharmacology

institute: UCLA

type: Genome binding/occupancy profiling by array

type: Genome binding/occupancy profiling by genome tiling array


title: Tumor-derived Jagged1- and Notch-dependent transcription changes in MC3T3-E1 osteoblasts

status: Public on Aug 15 2010

city: Princeton

first: Yibin

last: Kang

state: NJ

address: LTL 254, Washington Road

department: Molecular Biology

institute: Princeton University

summary: Transcriptional profiling of MC3T3-E1 osteoblasts that were flow cytometry-separated from cocultures with control or Jagged1-overexpressing tumor cells and treated with either DMSO control or 1μM MRK-003 (gamma-secretase inhibitor).

overall_design: One cell line (MC3T3-E1) cells: four different experimental conditions: cultured with (1) control tumor cells + DMSO; (2) Jagged1-overexpressing tumor cells + DMSO; (3) control tumor cells + MRK-003; (4) Jagged1-overexpressing tumor cells + MRK-003. Each experiment has two biological replicates. Total, 8 samples.

first: Nilay

last: Sethi


title: Murine postnatal subventricular zone (SVZ) neural stem cells (NSCs): Wild-type (WT) vs. Dnmt3a-null (KO)

summary: Transcriptional profiling of mouse postnatal SVZ NSCs comparing WT NSCs with KO NSCs under proliferating/undifferentiated states as well as differentiating conditions. Goal was to determine Dnmt3a-dependent gene expression changes in postnatal SVZ NSCs

overall_design: Two-condition experiment with a dye-swap design, WT NSCs vs. KO NSCs. Biological replicates: 4 replicates under proliferating/undifferentiation conditions, 2 replicates under differentiating conditions.

first: Hao

last: Wu

first: Volkan

last: Coskun

first: Jifang

last: Tao

first: Wei

last: Xie

first: Weihong

last: Ge

first: Kazuaki

last: Yoshikawa

first: En

last: Li

last: Zhang


title: Microarray analysis in Npc1-/- mouse cerebellum

city: Shanghai

first: Leming

last: Shi

address: 2005 Songhu Road

department: School of Life Sciences

institute: Fudan University

summary:
Niemann-Pick Type C disease is an autosomal recessive neurodegenerative disorder with abnormal lipid storage as the major cellular pathologic hallmark. Genetic analyses have identified mutations in NPC1 gene in the great majority of cases, while mutations in NPC2 account for the remainders. Yet, little is known regarding the cellular mechanisms responsible for NPC pathogenesis, especially for neurodegeneration, which is the usual cause of death.
To identify critical steps that could account for the pathological manifestations of the disease in one of the most affected brain structures, we performed global gene expression analysis in the cerebellum from three-week old Npc1+/+ and Npc1-/- mice with two different microarray platforms (Agilent and Illumina). Our results provide novel molecular insight regarding the mechanisms of pathogenesis in NPC disease and reveal potential new therapeutic targets.

overall_design: We performed global gene expression analysis in the cerebellum from three-week old Npc1+/+ and Npc1-/- mice with two different microarray platforms (Agilent and Illumina). Differentially-expressed genes identified by both microarray platforms were then subjected to KEGG pathway analysis. Expression of genes in six pathways was significantly altered in Npc1-/- mice; functionally, these signaling pathways belong to the following three categories: 1) steroid and terpenoid biosynthesis, 2) immune response, and 3) cell adhesion/motility. In addition, the expression of several proteins involved in lipid transport was significantly altered in Npc1-/- mice.

first: Guanghong

last: Liao

first: Zhining

last: Wen

first: Kristopher

last: Irizarry

first: Ying

last: Huang

first: Katherine

last: Mitsouras

first: Mariam

last: Darmani

first: Terry

last: Leon

first: Xiaoning

last: Bi


title: Gene Expression upon Doxorubicin Treatments

status: Public on Jul 15 2010

city: Durham

first: ASHUTOSH

last: CHILKOTI

address: BME, PO Box 90281, Duke University

department: BME

institute: Duke University

summary: Murine C26 tumor xenografts displayed different responses to the treatments of PBS, Doxorubicin (Dox), and chimeric polypeptide (CP)-Dox conjugates. We used microarrays to globally study gene expression underlying these different responses and identified distinct classes of up-regulated or down-regulated genes upon treatment.

overall_design: C26 murine colon carcinoma xenografts were analyzed at 48 hours after treatment with CP-Dox, free Dox, and PBS (control). This study involved four replicates of each treatment.

first: Jonathan

middle: R

last: McDaniel

first: J

last: MacKey

first: Mingnan

last: Chen

first: Ashutosh

last: Chilktoi


title: Uterine Gene Profile of Estriol, a Weak Estrogen

status: Public on Sep 09 2010

city: RTP

first: NIEHS

last: Microarray Core

department: DIR

summary: Females were ovariectomized and injected with saline estradiol or estriol. Uterine tissue was collected after 2 or 24 hours. RNA was analyzed by microarray compare ealry and late responses to a potent and a weak estrogen agaonist.

overall_design: 3 uteri per group were analyzed individually on one-color Agilent arrays.

first: Sylvia

last: Hewitt

first: Kevin

last: Gerrish

first: Kenneth

last: Korach


title: Expression data of primary melanocytes from aryl hydrocarbon deficient mice and corresponding wild-type C57BL/6 mice

status: Public on Sep 05 2010

city: Dusseldorf

first: Charlotte

last: Esser

address: Auf´m Hennekamp 50

department: Molecular Immunology

institute: IUF

summary:
[original Title] Comparison of expression data of primary murine melanocytes from aryl hydrocarbon deficient mice and corresponding wild-type C57BL/6 mice

Melanin is produced exclusively by melanocytes and melanogenesis is the vital response to protect skin cells against Ultraviolet B (UVB)-induced DNA damage. The aryl hydrocarbon receptor (AhR) is a transcription factor, which may be involved in the physiological tanning response. Normal murine melanocytes express functional AhR. We tested gene expression in WT versus AhR-deficient mice primary murine melanocytes, isolated from the skin and cultivated for several passages.

overall_design: Skin epidermal cells from 2 individual C57BL/6 mice and 2 individual AhR-deficient mice (deletion of exon2, AhRtm1Bra)  were grown for 6-8 weeks in selection medium to propagate melanocytes.

first: Bettina

last: Jux


title: Regulatory Role for PC-TP/StarD2 in the Metabolic Response to Peroxisome Proliferator Activated Receptor Alpha (PPARα)

status: Public on Aug 12 2010

city: Boston

first: hyewon

last: kang

address: 75 Fransis street

institute: Brigham & Women's Hospital

summary: Phosphatidylcholine transfer protein (PC-TP, a.k.a StarD2) is abundantly expressed in liver and is regulated by PPARα.  When fed the synthetic PPARα ligand fenofibrate, Pctp-/- mice exhibited altered lipid and glucose homeostasis.  Microarray profiling of liver from fenofibrate fed wild type and Pctp-/- mice revealed differential expression of a broad array of metabolic genes, as well as their regulatory transcription factors.  Because its expression controlled the transcriptional activities of both PPARα and HNF4α in cell culture, the broader impact of PC-TP on nutrient metabolism is most likely secondary to its role in fatty acid metabolism.

overall_design: 6 livers collected from PC-TP knockout mice fed a fenobrate-supplemented diet were used as the experimental group.  6 livers collected from wild type mice fed a fenofibrate-supplemented diet were used as the control group.  RNA prepared from one liver was used to hybridize one GeneChip, so that there were 6 experimental GeneChips and 6 control GeneChips.

first: David

last: Cohen

first: Hye

last: Kang

first: Keishi

last: Kanno


title: Gene expression analysis of fetal liver pro-B cells upon deletion of Early B-cell Factor 1 (Ebf1)

status: Public on Jun 24 2010

city: Freiburg

first: Rudolf

last: Grosschedl

address: Stuebeweg 51

department: Cellular and Molecular Immunology

institute: Max Planck Institute of Immunobiology

summary: Using cultured pro-B cells from mice carrying two Ebf1 alleles flanked with loxP sites and an inducible Cre recombinase, target genes of Ebf 1 and the effect of Ebf1 deletion on the cells was analyzed

overall_design: Ebf1 fl/fl pro-B cells and heterozygote control cells were treated with 4-hydroxy-tamoxifen (4OHT) for 24 h to activate an ER-Cre fusion protein. Four days after treatment no Ebf1 expression could by detected and RNA was extracted for expression analysis.

first: Ildiko

last: Györy


title: Expression data from Hif 2alpha Knockdown study

status: Public on Jun 28 2010

city: Philadelphia

first: Dhruv

middle: K

last: Pant

state: PA

address: 421 Curie Blvd.

institute: University of Pennsylvania

summary:
Non-small cell lung cancer (NSCLC) is the leading cause of cancer deaths worldwide.  The oxygen-sensitive Hypoxia Inducible Factor (HIF) transcriptional regulators HIF-1α and HIF-2α are overexpressed in many human NSCLCs, and constitutive HIF-2α activity can promote murine lung tumor progression, suggesting that HIF proteins may be effective NSCLC therapeutic targets. To investigate the consequences of inhibiting HIF activity in lung cancers, we deleted Hif-1α or Hif-2α in an established KrasG12D-driven murine NSCLC model.  Deletion of Hif-1α had no obvious effect on tumor growth, whereas Hif-2α deletion resulted in an unexpected increase in tumor burden that correlated with reduced expression of the candidate tumor suppressor gene Scgb3a1 (HIN-1).
Here, we identify Scgb3a1 as a direct HIF-2α target gene, and demonstrate that HIF-2α regulates Scgb3a1 expression and tumor formation in human KrasG12D-driven NSCLC cells.  AKT pathway activity, reported to be repressed by Scgb3a1, was enhanced in HIF-2α deficient human NSCLC cells and xenografts.  Finally, a direct correlation between HIF-2α and SCGB3a1 expression was observed in approximately 70% of human NSCLC samples analyzed. These data suggest that whereas HIF-2α overexpression can contribute to NSCLC progression, therapeutic inhibition of HIF-2α below a critical threshold may paradoxically promote tumor growth by reducing expression of tumor suppressor genes, including Scgb3a1.

overall_design: RNA was isolated from tumors of experimental (Hif2alpha deficient) mice and control mice (seven for each group).

first: Jolly

last: Mazumdar

first: Michele

middle: M

last: Hickey

first: Amy

last: Durham

first: Alejandro

last: Sweet-Cordero

first: Anil

last: Vachani

first: Tyler

last: Jacks

first: Lewis

last: Chodosh

first: Joseph

last: Kissil

first: M

last: Simon

first: Brian

last: Keith


title: Expression data from lung adenocarcinoma mouse tumors

status: Public on Jun 18 2010

city: Burjassot

first: Julian

last: Carretero

state: Valencia

address: Ave. Vicent Andres Estelles s/n

department: Physiology

country: Spain

institute: University of Valencia

summary:
To identify altered signal transduction pathways involved in the progression and metastases of Lkb1 deficient lung  tumors, we have performed an unbiased microarray analysis of primary and metastatic mouse lung tumors
We used microarrays to detail the global programme of gene expression underlying metastatic progression

overall_design: We compared RNA expression profiles from 9 Kras and 9 Kras/Lkb1 primary tumors as well as 17 Kras/Lkb1 metastases (lymph node and distant sites)

first: Kwok-kin

last: Wong


title: Control of oligodendroglial cell number by the miR-17~92 family of miRNA cluster (mRNA profiling)

status: Public on Jun 01 2010

city: Goettingen

first: Gabriela

last: Salinas

state: Lower-Saxony

address: Kreuzbergring 57

department: Department of Pathology

institute: Universitaetsmedizin Goettingen

summary: The generation of myelinating cells in the central nervous system (CNS) requires the initiation of specific gene-expression programs in oligodendrocytes. We reasoned that miRNAs could play an important role in this process by regulating critical developmental genes. Microarray profiling of cultured oligodendrocytes identifies the miR-17~92 family of miRNA cluster as highly enriched miRNAs in oligodendrocytes.We specifically deleted the miR-17~92 cluster in oligodendrocytes using the 2´3´-cyclic nucleotide 3´-phosphodiesterase (CNP)-Cre mice. Absence of miR-17~92 leads to a reduction of oligodendrocyte number in vivo and we find that the expression of these miRNAs in primary cultures of oligodendrocytes promotes cell proliferation by influencing Akt signalling. Together, these results suggest that the miRNA pathway is essential in determining oligodendroglial cell number and that the miR-17~92 cluster is crucial in this process.

overall_design: Transcriptome microarray profiling was used for the identification of mRNAs enriched in oligodendrocytes. Total RNA lysates from primary oligodendroctes compared to primary astrocytes were analysed regarding their mRNA levels. Three independent samples for each of the two cell types were used. The study was initially designed with a comparison of oligodendrocytes, astrocytes and microglia. However, only the comparison of oligodendrocytes and astrocytes is discussed in the present study.

first: Holger

last: Budde

first: Sebastian

last: Schmitt

first: Dirk

last: Fitzner

first: Lennart

last: Opitz

last: Salinas-Riester

first: Mikael

last: Simons


title: Gene expression in LPS stimulated IkappaB-beta knockout bone marrow derived macrophage (BMDM)

status: Public on Jun 09 2010

city: New York

first: Ping

last: Rao

department: Microbiology and Immunology

institute: Columbia University

summary: Inflammation is beneficial when it is part of the innate immune response, but harmful when it occurs in an unregulated, chronic manner. We now report that IkappaB-beta, a member of the classical IkappaB family, serves a dual role of both inhibiting and facilitating the inflammatory response. IkappaB-beta degradation releases NF-kappaB dimers which upregulate proinflammatory target genes such as TNF-alpha. Suprisingly absence of IkappaB-beta results in a dramatic reduction of TNF-alpha in response to LPS even though the activation of NF-kappaB is normal. The inhibition of TNF-alpha mRNA expression can be correlated to the absence of nuclear, hypophosphorylated-IkappaB-beta bound to p65:cRel heterodimers at a specific kappaB site on the TNF-alpha promoter. Therefore IkappaB-beta acts through p65:cRel dimers to maintain prolonged expression of TNF-alpha. As a result, IkappaB-beta knockout mice are resistant to LPS induced septic shock and collagen-induced arthritis, and therefore blocking IkappaB-beta might be a promising new strategy for selectively inhibiting the chronic phase of TNF-alpha producting during the inflammatory response.

overall_design: Wild type and IkappaB-beta knockout BMDM cells were stimulated with LPS(1ug/ml) for 0, 1, and 5 hours. RNA isolated from the cells was analyzed on Affymetrix Mouse Genome 430A 2.0 gene expression chip.

first: Sankar

last: Ghosh


title: Serotonin stimulation of alveolar macrophages from wild type and 5-HT2C deficient animals

status: Public on May 31 2010

city: Giessen

first: Jochen

last: Wilhelm

address: Gaffkystrasse 10

department: ECCPS Microarray Unit

institute: Uniklinikum Giessen

summary:
Gene regulation upon serotonin stimulation was compared in wild-type and 5HT2C receptor kock-out mice.

Serotonin (5-HT), known as neuromodulator, regulates immune responses and inflammatory cascades. The expression and function of 5-HT receptors on alveolar macrophages (AM), which are the major fraction of pulmonary immune cells, remain elusive. Therefore we determined the expression of 5-HT type 2 receptors and investigated the effects evoked by stimulation with 5-HT in AM compared to alveolar epithelial cells (AEC). Quantitative PCR (qPCR) analysis revealed expression of the receptors 5-HT2A and 5-HT2B in AEC and of 5-HT2C in AM. In AM, 5-HT (10-5 M) induced a rise in intracellular calcium concentration ([Ca2+]i) that was initiated by release of Ca2+ from intracellular stores and depended on extracellular Ca2+ in a sustained phase. This 5-HT-induced increase in [Ca2+]i was not observed in AM treated with the 5-HT2C-selective inhibitor RS102221 and in AM derived from 5-HT2C-deficient mice. AM stimulated with 5-HT (10-5 M) showed increased expression of CCL2 (MCP-1) mRNA as assayed by qPCR at 4 h and augmented production of CCL2 protein as determined by dot-blot assay and ELISA at 24 h. Notably, in 5HT2C-deficient AM, CCL2 production was not affected by 5-HT treatment. Moreover, transcriptional responses to 5-HT exposure assayed by microarray experiments were only observed in AM from wild type animals but not in AM derived from 5-HT2C-deficient mice.
Taken together these data demonstrate the presence of functional 5-HT2C receptors on AM and suggest a role of 5-HT as novel modulator of AM function. These effects are exclusively driven by the 5-HT2C receptor, thereby providing the potential for selective intervention.

overall_design: primary isolated murine alveolar macrophages were stimulated with serotonin

first: Zbigniew

last: Zaslona

last: Mikulski

first: Lidija

last: Cakarova

first: Petra

last: Hartmann

first: Laurence

last: Tecott

first: Juergen

last: Lohmeyer

first: Wolfgang

last: Kummer


title: Gene expression analysis after reconstitution of Ebf1-deficient pre-pro-B cells with Ebf1

first: Rudolf

last: Grosschedl

summary: Ebf1 deficient pre-pro B-cells (Fraction A) can be cultured in the presence of stromal feeders and cytokines. The retroviral transduction of these cells with Ebf1 was used as gain-of-function experiment for the analysis of direct and functional target genes of Ebf1.

overall_design: Ebf1 deficient pre-pro B-cells were retrovirally transduced with an Ebf1-expressing or control retrovirus. 24h after transduction the infected cells were isolated and their gene expression profile was compared.

first: Elizabeth

last: Mandel

first: Thomas

last: Treiber


title: Control of oligodendroglial cell number by the miR-17~92 family of miRNA cluster

first: Gabriela

last: Salinas

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

platform_organism:
Homo sapiens
Mus musculus
Rattus norvegicus
Human alphaherpesvirus 1
Human betaherpesvirus 5
human gammaherpesvirus 4
JC polyomavirus
Human immunodeficiency virus 1
Human gammaherpesvirus 8
Betapolyomavirus hominis
Betapolyomavirus macacae

overall_design: Refer to individual Series


title: Identification of genes regulated by the phosphotylation of PPARgamma

status: Public on May 28 2010

first: Jang Hyun

last: Choi

state: MA

address: 44 Binney st

institute: Dana-Farber Cancer Institute

summary: In order to identify the molecular mechanisms of PPARgamma phosphorylation at Set273, we generated cell-lines of PPARgamma KO MEFs expressing wtPPARgamma or S273APPARgamma. In addition, because our data showed that PPARgamma ligand drugs such as rosiglitazone and MRL24 blocked this phopshorylation, we treated cells with these drugs, then prepared RNA samples to look at the gene profiling.

overall_design: PPARgamma KO MEFs were introduced by wtPPARgamma or S273APPARgamma. Cells were differentiated for 6 days. Then, wtPPARgamma-introduced KO MEFs were treated with either 1 uM rosiglitazone or 1uM MRL24 for 24h. Cells were harvested and we purified total RNA samples.

first: Jang-Hyun

first: Bruce

last: Spiegelman


title: A constitutively activated form of the p110 beta isoform of PI3-kinase induces prostatic intraepithelial neoplasia in mice

status: Public on May 20 2010

first: Sang Hyun

last: Lee

address: 44 Binney Street, SM970

department: Cancer Biology

summary: The global gene expression profiles of ventral prostates of wild type mice and p110 beta transgenic mice.

overall_design: normal prostate vs. prostate cancer induced by the overexpression of the active allele of p110 beta

first: S

first: T

last: Roberts


title: PRONOUNCED PHENOTYPE IN ACTIVATED TREG CELLS DURING A CHRONIC HELMINTH INFECTION

status: Public on Mar 31 2010

city: Erlangen

first: Roland

last: Lang

address: Wasserturmstr. 3-5

institute: University Hospital Erlangen

summary: Although several markers have been associated with the characterization of regulatory T cells (Treg) and their function, no studies have investigated the dynamics of their phenotype during infection. Since the necessity of Treg to control immunopathology has been demonstrated, we used the chronic helminth infection model S. mansoni to address the impact on the Treg gene repertoire. Before gene expression profiling we first chose to study the localization and antigen-specific suppressive nature of classically defined Treg during infection. Presence of Foxp3+ cells were found especially in the periphery of granulomas and isolated CD4+CD25hiFoxp3+ Treg from infected mice blocked IFN-gamma and IL-10 cytokine secretion from infected CD4+CD25- effector T cells (Teff). Furthermore the gene expression patterns of Treg and Teff showed that in total 474 genes were significantly regulated during chronic schistosomiasis. Upon k-means clustering we identified genes exclusively regulated in all four populations including Foxp3, CD103, GITR, OX40 and CTLA-4: classical Treg markers. During infection however, several non-classical genes were up-regulated solely within the Treg population such as Slpi, Gzmb, Mt1, Fabp5, Nfil3, Socs2, Gpr177 and Klrg1. Using RT-PCR we confirmed aspects of the microarray data and in addition showed that the expression profile of Treg from S. mansoni-infected mice is simultaneously unique and comparative with Treg derived from other infections

overall_design: Regulatory T cells (Treg) or effector T cells (Teff) were FACS-sorted as CD4+CD25+ or CD4+CD25- from mesenteric lymph nodes (MLN) of naive mice or from mice infected with Schistosoma mansoni. Affymetrix MOE430A 2.0 genechips were used to identify genes differentially expressed in Treg or Teff under resting or infected conditions.

first: Laura

last: Layland


title: Lgr6 Marks Stem Cells in the Hair Follicle that Generate all Cell Lineages of the Skin

status: Public on Mar 26 2010

city: Dresden

first: Daniel

middle: E.

last: Stange

address: Fetscherstr. 74

institute: University Clinic Dresden

summary: Mammalian epidermis consists of three self-renewing compartments: the hair follicle, sebaceous gland and interfollicular epidermis. We generated knock-in alleles of murine Lgr6, a close relative to the Lgr5 stem cell gene. Lgr6 was expressed in the earliest embryonic hair placodes. In adult hair follicles, Lgr6+ cells resided in a previously uncharacterized region directly above the follicle bulge. They expressed none of the known bulge stem cell markers. Prenatal Lgr6+ cells established the hair follicle, sebaceous gland and interfollicular epidermis. Postnatally, Lgr6+ cells generated sebaceous gland and interfollicular epidermis, while contribution to hair lineages gradually diminished with age. Adult Lgr6+ cells executed long-term wound repair, including the formation of new hair follicles. We conclude that Lgr6 marks the most primitive epidermal stem cell.

overall_design: For the Lgr5 and Lgr6 stem cell comparison RNA was isolated from sorted GFPhi cell fractions of dorsal skin from Lgr5-EGFP-ires-CreERT2 mice and Lgr6-EGFP-ires-CreERT2, respectively (3 mice per group per sort).

first: Hugo

last: Snippert

first: Marc

last: vandeWetering

first: Hans

last: Clevers


title: Gene expression in mice brain after ciguatoxin exposure

city: Charleston

first: Jimmy

last: Ryan

state: SC

address: 331 Fort Johnson Rd

department: Marine Biotoxins

institute: NOAA

summary: This study characterizes the global transcriptional response in mouse brain to a symptomatic dose (0.26 ng/g) of the highly toxic Pacific ciguatoxin P-CTX-1 at 1, 4 and 24 hrs using whole genome microarrays

overall_design: Two-condition experiment, ciguatoxin treated vs vehicle treated mice. 9 Biological replicates: 9 control replicates, pooled into 3 control time points.

first: James


title: Gene expression induced by trace fear conditioning in murine hippocampus

status: Public on May 06 2010

city: Milan

first: Daniela

last: Toniolo

address: Via Olgettina, 58

department: Dibit

country: Italy

institute: San Raffaele Scientific Institute

summary:
Gene expression profiling following different learning paradigms may help in defining the moleular pathways of memory formation. In this study we analyzed the gene expression pattern of murine hippocampus at different time points (0.5 h, 2h, 6h) after trace fear conditioning. We compared trained mice with  naive mice that remained in their homecages.

Keywords: Time course

overall_design: We used 3 arrays for each experimental condition. Each array was hybridized witha a pool of RNA of 6 animals.