title: Gene expression profiling of the palate in Erk2 mutant mouse models

status: Public on Dec 11 2015

city: Oklahoma City

first: Richard

last: Pelikan

state: Oklahoma

address: 825 NE 13th St

department: Genes & Human Disease Research Program

institute: Oklahoma Medical Research Foundation

summary: The overall goal of this project is to investigate the role of Erk2-mediated signaling in regulating the cellular metabolism of cranial neural crest (CNC) cells during palate development. Here, we conducted gene expression profiling of palate tissue from wild type mice as well as those with a neural crest specific conditional inactivation of the Erk2 gene. The latter mice exhibit micrognathia, tongue defects and cleft palate, which is among the most common congenital birth defects and observed in many syndromic conditions.

overall_design: To investigate the adverse effects of dysfunctional ERK signaling  on the cellular metabolism of palatal mesenchyme during palatogenesis, we analyzed mice with a neural crest cell-specific conditional inactivation of Erk2 (Erk2fl/fl;Wnt1-Cre). We performed microarray analyses of primary mouse embryonic palatal mesenchymal cells of Erk2fl/fl;Wnt1-Cre mutant mice and Erk2fl/fl control mice, collected at embryonic day 13.5 (n=3 per genotype) and E14.5 (n=5 per genotype).

first: Carolina

last: Parada

first: Yang

last: Chai


title: Mouse bone marrow Mesenchymal Stem Cells (MSC) exposed to activated T cells

status: Public on Dec 08 2015

city: Genoa

first: Tiziana

last: Vigo

address: Largo Daneo

country: Italy

institute: University of Genoa

summary:
To analyze the changes induced in MSC transcriptome by activated T cells, MSC were co-cultured in transwell with anti CD3/CD28 activated T cells for 48 hrs before RNA extraction
IFNγ-induced plasticity of mesenchymal stem cells is regulated by STATs through inhibition of mTOR and TGFβ pathways. Vigo T, Procaccini C, Ferrara G, Baranzini S, Oksenberg J, Diaspro A, Kerlero de Rosbo N, Uccella A.

overall_design: The expression of MSC co-cultured with activated T cells ( two replicates) were compared to that of naive MSC (3 replicates)

first: Antonio

last: Uccelli

first: Sergio

last: Baranzini

first: Enrico

last: Pedemonte


title: Differential Ly6C Expression after Renal Ischemia-Reperfusion Identifies Unique Macrophage Populations

status: Public on Dec 09 2015

city: Framingham

first: Anna

last: Zuk

state: MA

address: 49 New York Ave

department: R&D

country: USA

institute: Genzyme

summary:
Macrophages are a heterogeneous cell type implicated in injury, repair, and fibrosis after AKI, but the macrophage population associated with each phase is unclear.results of this study in a renal ischemia-reperfusion injury model allow phenotype and function to be assigned to CD11b+/Ly6C+ monocyte/macrophage populations in the pathophysiology of disease after AKI.
we used a renal bilateral ischemia-reperfusion injury mouse model to identify unique monocyte/macrophage populations by differential expression of Ly6C in CD11b+ cells and to define the function of these cells in the pathophysiology of disease on the basis of microarray gene signatures and reduction strategies

overall_design: Macrophage populations were sorted by Flow Cytometry into low and intermediate populations by Itgam(Cd11b) and Ly6c markers. The cells obtained in 5 weeks sham, 5 weeks IR, 9 day sham, and 9 day IR with 6 samples per group (3 int and 3 low). Cells were sorted in 350ul of RLT lysing buffer and kept at -80c until RNA extraction.Sample amplification, fragmentation, hybridization,washing and scanning were performed according to validated Affymetrix protocol in a CLIA certified lab.

first: Meghan

last: Clements

first: Michael

last: Gershenovich

first: Christopher

last: Chaber

first: Juanita

last: Campos-Rivera

first: Pan

last: Du

first: Mindy

last: Zhang

first: Steve

last: Ledbetter


title: Reduced adult neurogenesis and neuronal abnormalities in the hippocampus underlie cognitive deficiency following prenatal administration of the anti-epileptic drug valproic acid

city: Shinagawa-ku

first: KATSUHIDE

last: IGARASHI

state: Tokyo

department: Life Science Tokyo Advanced Research center (L-StaR)

country: Japan

institute: Hoshi University School of Pharmacy and Pharmaceutical Science

summary: Prenatal exposure to valproic acid, an established anti-epileptic drug, has been reported to impair postnatal cognitive function of children from epileptic mothers. Nevertheless, its pathology and proper treatment to minimize the effects remain unknown. In mice, we found that the postnatal cognitive function impairment was mainly caused by a reduction of adult neurogenesis and abnormal neuronal features in the hippocampus, which could be ameliorated by voluntary running.

overall_design: Pregnant mice received an oral administration of methylcellulose (MC), valproic acid (VPA) or valpromide (VPM) once a day on three consecutive embryonic days (E) 12.5, E13.5, and E14.5 and were sampled 3hr after the last administration (E14.5), at E18.5, and at 12 weeks of age.

first: Berry

last: Juliandi

first: Katsuhide

last: Igarashi

first: Kinichi

last: Nakashima


title: Comparison of prostate epithelial cells from intact and castrated mice

status: Public on Dec 03 2015

city: Los Angeles

first: Andrew

middle: Scott

last: Goldstein

state: CA

address: 610 Charles E Young Dr East

department: Urology

institute: University of California, Los Angeles

summary: Androgen is critical for the growth of the murine prostate. Castration removes the predominant source of androgen in the mouse, leading to prostatic atrophy and death of epithelial cells. However, studies show that epithelial cells which remain in the castrated prostate are enriched for progenitor activity compared to the intact prostate. We performed gene expression profiling of basal and luminal epithelial cells isolated from paired intact and castrated adult male C57BL/6 mouse prostates to gain insights into the mechanisms promoting survival in castration-resistant epithelial cells.

overall_design: 3 distinct sets (biological replicates) of adult male (8 weeks) C57BL/6 mice were subjected to surgical orchiectomy (castration) or remained intact. Four weeks post castration, castrated and paired intact animals were sacrificed and epithelial subsets were isolated from dissociated prostate tissues using fluorescence activated cell sorting. Luminal cells have the antigenic profile Lin- CD49f(lo) EpCAM+ and basal cells have the antigenic profile Lin- CD49f(hi) EpCAM+.

middle: S

first: Owen

middle: N

last: Witte


title: Identification of a New Cell Population Constitutively Circulating in Healthy Conditions and Endowed with a Homing Ability Toward Injured Sites

status: Public on Dec 04 2015

city: Genova

first: Ulrich

last: Pfeffer

address: L. Benzi 10

institute: IRCCS AOU San Martino - IST

summary: Stem and progenitor cells are the critical units for tissue maintenance, regeneration, and repair. The activation of regenerative events in response to tissue injury has been correlated with mobilization of tissue-resident progenitor cells, which is functional to the wound healing process. However, until now there has been no evidence for the presence of cells with a healing capacity circulating in healthy conditions. We identified a rare cell population present in the peripheral blood of healthy mice that actively participates in tissue repair. These Circulating cells, with a Homing ability and involved in the Healing process (CH cells), were identified by an innovative flowcytometry strategy as small cells not expressing CD45 and lineage markers. Their transcriptome profile revealed that CH cells are unique and present a high expression of key pluripotency- and epiblast-associated genes. More importantly, CH-labeled cells derived from healthy Red Fluorescent Protein (RFP)-transgenic mice and systemically injected into syngeneic fractured wild-type mice migrated and engrafted in wounded tissues, ultimately differentiating into tissue-specific cells. Accordingly, the number of CH cells in the peripheral blood rapidly decreased following femoral fracture. These findings uncover the existence of constitutively circulating cells that may represent novel, accessible, and versatile effectors of therapeutic tissue regeneration.

overall_design: Analysis of murine circulating PlCH cells, two biological replicates

first: Claudia

last: Lo Sicco


title: Novel transcriptome signatures and markers defining murine macrophages at the extremes of the canonical M1 and M2 polarization spectrum

city: Columbus

first: Mireia

last: Guerau

state: OH

address: 453 W 10th Ave

department: HRS-Medical Laboratory Science

institute: The Ohio State University

summary: Classically (M1) and alternatively activated (M2) macrophages play distinct roles in various physiological and disease processes. Understanding the gene transcription programs that contribute to macrophage polarization along the M1/M2 spectrum may lead to new tools to detect and therapeutically manipulate macrophage phenotype. Here, we define the M1 and M2 macrophage signature through mRNA microarray. The M1 macrophage signature was defined by 629 up-regulated and 732 down-regulated genes while the M2 macrophage signature was formed by 388 up-regulated and 425 down-regulated genes. While a subset of probes was common to both M1 and M2 cells, others were exclusive to each macrophage subset. The common M1/M2 pathways were characterized by changes in various transcriptional regulators and signaling partners, including increases in Kruppel-like Factor (Klf) 4, but decreases in Klf2. To identify M1 and M2 biomarkers that help discriminate these populations, we selected genes that were increased during M1 or M2 differentiation but decreased in the opposite population. Among top novel M1-distinct genes, we identified CD38, G-protein coupled receptor 18 (Gpr18) and Formyl peptide receptor 2 (Fpr2). Among top M2 genes, we found early growth response protein 2 (Egr2) and Myc. We validated these genes by Real-Time PCR and developed a CD38/Egr2-based flow cytometry assay that discriminates between M1 and M2 macrophages. Overall, this work defines the M1 and M2 signature and identifies several novel M1 and M2 genes that may be used to distinguish and manipulate M1 and M2 macrophages.

overall_design: Total RNA was prepared from bone marrow-derived macrophages of wild-type mice (n=2-3 independent mice) treated in M0, M1 or M2 conditions (n=2-3  replicates per condition originating from different mice)

last: Guerau-de-Arellano


title: Expression profiles of murine FOXO1+/+ and FOXO1-null GC B cells

city: New York

first: Riccardo

last: Dalla-Favera

state: NY

address: 1130 St Nicholas Avenue

institute: Columbia University

summary:
The pathways regulating the formation of the germinal center (GC) dark- (DZ) and light- (LZ) zones are unknown. We show that FOXO1 expression is restricted to the GC DZ and is required for DZ formation, since its absence in mice leads to the complete loss of DZ gene programs and the formation of LZ-only GCs. FOXO1-negative GC B-cells display normal somatic hypermutation, but defective affinity maturation and class switch recombination. The function of FOXO1 in sustaining the DZ program involves the transactivation of the chemokine receptor CXCR4, and the cooperation with BCL6 in the trans-repression of genes involved in immune activation, DNA-repair and plasma cell differentiation. These results have also implications for understanding the role of FOXO1 mutations in lymphomagenesis.
We used microarrays to determine the consequences of FOXO1 deletion in the GC B cell comparment, and correlate these data with phenotypic changes

overall_design: GC B cell subpopulations were collected by Fluorescence Activated Cell Sorting (FACS) from B cell enriched fractions of splenic mononuclear cell pools  (12 days after SRBC immunization). 20ng of total RNA (RIN>9) for each sample was used as a template for linear cDNA amplification (Ovation RNA amplification Kit, NuGen). cDNA was labeled using the Encore Biotin Labeling Kit (NuGen) and hybridized to Affymetrix Mouse 430.2 gene expression arrays

first: David

last: Dominguez-Sola

first: Katia

last: Basso

first: Antony

last: Baden Holmes


title: Brg1 Coordinates Multiple Processes During Retinogenesis and is a Tumor Suppressor in Retinoblastoma

status: Public on Dec 02 2015

city: Memphis

last: Finkelstein

state: TN

address: 332 N. Lauderdale St.

department: Computational Biology

institute: St Jude Children's Research Hospital

summary: Retinal development requires precise temporal and spatial coordination of cell cycle exit, cell-fate specification, cell migration and differentiation.  When this process is disrupted, retinoblastoma, a developmental tumor of the retina, can form. Epigenetic modulators are central to precisely coordinating developmental events, and many epigenetic processes have been implicated in cancer. Studying epigenetic mechanisms in development is challenging because they often regulate multiple cellular processes; therefore, elucidating the primary molecular mechanisms involved can be difficult. Here we explore the role of Brg1 in retinal development and retinoblastoma by using molecular and cellular approaches. Brg1 regulated retinal size by controlling cell cycle length, cell cycle exit, and cell survival during development. Brg1 was not required for cell-fate specification but was required for photoreceptor differentiation and cell adhesion/polarity programs that contribute to proper retinal lamination during development. The combination of defective cell differentiation and lamination led to retinal degeneration in Brg1-deficient retinae. Despite the hypocellularity, premature cell cycle exit, increased cell death, and extended cell cycle length, retinal progenitor cells persisted in Brg1-deficient retinae, thereby making them more susceptible to retinoblastoma. ChIP-seq analysis provided insight into the underlying molecular mechanisms of these complex Brg1-regulated cellular processes during retinal development.

overall_design: mouse BRG1 -/- retinae from mice were compared to controls at distinct time points in embryonic and post-natal development

first: Issam

last: AlDiri

first: Itsuki

last: Ajioka

first: Beisi

last: Xu

first: Jiakun

first: Xiang

last: Chen

last: Benavente

first: Dianna

last: Johnson

first: Jennifer

last: Akiyama

first: Len

last: Pennacchio

first: Michael

last: Dyer


title: Differential gene expression following SCI in trkB.T1 null

status: Public on Dec 07 2015

city: Baltimore

first: Susan

middle: G

last: Dorsey

address: 655 West Lombard Street

department: Pain and Translational Symptom Science

institute: University of Maryland Baltimore

summary:
We asked what genes are significantly differentially regulated in the spinal cord of SCI trkB.T1 WT and trkB.T1 KO mice. TrkB.T1 is upregulated shortly after SCI although the precise mechanisms underyling this upregulation are poorly understood. In the trkB.T1 null, we show less mechanical allodynia and better locomotor recovery following SCI. The microarray studies helped us to elucidate a signaling pathway that is differently regulated in the WT versus KO mice at 1 day after SCI.
In this study, we did not examine gene changes within a genotype after SCI. Rather, we examined DGE by genotype at each time point.

overall_design: Spinal cord tissue from WT and KO mice in a sham condition (intact spinal cord) versus 1D, 3D and 7D following SCI was harvested for microarray analyses.

first: Alan

middle: I

last: Faden


title: Molecular distinctions between proprioceptors supplying Tibialis anterior (TA) and Gastrocnemius (GS) muscles [array]

first: Sebastian

last: Poliak

address: 701 West 168st

department: Neuroscience and Biochemistry and Molecular Biophysics

summary: Muscle-specific populations of proprioceptive sensory neurons form selective connections with spinal motor neurons, implying the existence of molecular distinctions between proprioceptor subpopulations. Here, we compare the gene expression profiles of proprioceptors that supply an antagonistic muscle pair functioning at a single hindlimb joint.

overall_design:
TA and GS muscles in a Pv::YFP reporter line were injected at p0  with ctb-555; retrogradely labeled  proprioceptors were manually isolated at p1 and pooled to form 25-30 neuron samples.
*** Processed data (i.e., Partek-generated log2 GCRMA signals) are unavailable. ***

first: Amy

last: Norovich

first: Thomas

last: Jessell


title: Expression data from Hand2 mutant mouse embryos

status: Public on Dec 15 2015

city: Bunkyo-ku

first: Noriko

last: Funato

address: 1-5-45 Yushima

institute: Tokyo Medical and Dental University

summary:
Acquisition of the lower jaw (mandible) was evolutionarily important for jawed vertebrates. In humans, syndromic craniofacial malformations often accompany jaw anomalies. Hand2 is involved in coordinating the developmental network of mandibles and the oral apparatus through Hand2-downstream genes and is therefore a major determinant of jaw identity.
We used microarrays to detail the global programme of gene expression involved in mandible specification and identified distinct classes of up-regulated genes during this process.

overall_design: Wild-type and Hand2 mutant (Hand2 CAT/+; Wnt1-Cre) embryos were collected at Embryonic day (E) 11.5 or E12.5 for RNA extraction and hybridization on Affymetrix microarrays.

first: Yumiko

last: Saga

first: Hiroki

last: Kokubo


title: PTH and PTHrP treatment of primary adipocytes

status: Public on Dec 01 2015

city: Boston

first: Serkan

last: KIR

address: 450 Brookline Ave

institute: Dana-Farber Cancer Inst.

summary: Parathyroid hormone (PTH) and PTH-related protein (PTHrP) are involved in cachexia associated with chronic kidney disease and cancer respectively. Tumor-derived PTHrP triggers adipose tissue browning and thereby leads to wasting of fat tissue in tumor-bearing mice. Similarly, elevated in 5/6 nephrectomized mice, PTH stimulates adipose tissue browning and wasting. Mice lacking the PTH/PTHrP receptor in their fat tissue are resistant to wasting of both adipose tissue and skeletal muscle. Therefore, the PTH/PTHrP signaling in adipocytes should activate various pathways that contribute to hypermetabolism and muscle wasting.

overall_design: Inguinal stroma-vascular fractions were cultured and differentiated into primary adipocytes. 8 days after differentiation, cells were treated with PTH(1-34) or PTHrP(1-34) (100 ng/ml each) for 4 hours.

last: Kir

first: Bruce

last: Spiegelman


title: GGTase-Iβ deletion in Intestinal Epithelial Cells

city: Erlangen

first: Rocío

last: López Posadas

address: TRC, Schwabachanlage 12

department: Medicine Clinic 1

country: Germany

institute: University of Erlangen-Nuremberg

summary:
Prenylation is a post-translational modification of proteins consisting on the attachment of a lipid residue (isoprenoid). GGTase-I is one of the prenyltransferases catalyzing prenylation.
Using mice with an inducible intestinal epihtelial cell specific deletion of GGTase-Iβ we analyzed the impact of geranylgeranylation within intestinal epithelium.

overall_design: Intestinal epithelial cells were isolated from 3 control mice and 3 mice with a codnitional deletion of GGTase-Iβ in Intestinal Epithelial Cells. RNA was isolated and subjected to Affymetrix gene chip analysis

last: López-Posadas

first: Imke

last: Atreya


title: Estrogen receptor alpha (ESR1)-dependent regulation of the mouse oviduct

status: Public on Nov 30 2015

city: Lexington

first: Phillip

middle: J

last: Bridges

state: KY

address: 206 WP Garrigus Building

department: Animal and Food Sciences

institute: University of Kentucky

summary: Estrogen receptor-α (ESR1) is an important transcriptional regulator in the mammalian oviduct, however ESR1-dependent regulation of this organ is not well defined, especially at the genomic level.  The objective of this study was therefore to investigate estradiol- and ESR1-dependent regulation of the transcriptome of the oviduct using transgenic mice, both with (ESR1KO) and without (wild-type, WT) a global deletion of this transcription factor using the Affymetrix Genechip Mouse Genome 430-2.0 arrays.

overall_design: Oviducts were collected from ESR1KO and WT littermates at 23 days of age, or ESR1KO and WT mice were treated with 5 IU PMSG to stimulate follicular development and the production of ovarian estradiol, and the oviducts collected 48 h later.  RNA extracted from whole oviducts was hybridized to Affymetrix Genechip Mouse Genome 430-2.0 arrays (n = 3 arrays per genotype and treatment).

first: K

middle: L

last: Cerny

first: P


title: Expression data for murine colon carcinoma cell line CT26.WT stimulated with S100a8 or S100a9 recombinant protein

status: Public on Nov 29 2015

city: Changsha

first: Xuemei

last: Zhang

address: xiangya road #110

country: China

institute: Key Laboratory of Carcinogenesis, Ministry of Health, China

summary: Damage-associated molecular pattern (DAMP) molecules S100A8 and S100A9 with well-known functions in inflammation, tumor growth and metastasis. It has been found to have promote tumor cell proliferation activity at low concentration . However, the mechanism underlying this remains unclear. In the current study, we performed genome expression profiling analysis using the Affymetrix genome wide microarray system to identify broad scale changes in gene expression associated with S100a8 or S100a9 recombinant protein stimulation in murine colon carcinoma cell line CT26.WT.

overall_design: Murine colon carcinoma cell line CT26.WT  cells exposed to serum-free medium for 12 hours, and then 4 ug/ml of S100a8 or S100a9 mouse recombinant protein  was added for an additional 24 hours respectively. Control serum-free medium was treated with normal saline. Total RNA were extracted and detected by Affymerix GeneChip® Mouse Genome 430 2.0 Array.

first: Feiyan

last: Ai

last: Li

first: Jian

last: Ma

first: Shourong

last: Shen


title: Identification of differential expressed genes among reprogrammed cells cultured under control condition and calcineurin-NFAT pathway inhibition condition at reprogramming day 3 and day 6 through genome-wide transcript profiling

city: Shanghai

first: Ming

last: Sun

address: 320 Yueyang Road

institute: Institute for Biological Sciences, Chinese Acadamy of Sciences

summary: Inhibition of calcineurin-NFAT pathway at the early stage can block somatic cell reprogramming. In order to study how the calcineurin-NFAT pathway contributes to the early stage of reprogramming, we designed this microarray experiment and tried to find out which genes or signalings were changed after inhibition of calcineurin-NFAT signaling by CSA (a specific inhibitor of calcineurin-NFAT pathway).

overall_design: We tried to compare gene profiling of different reprogrammed cells treated with DMSO and CSA (10 mM) at reprogramming day 3 and day 6 in our OSKM secondary reprogramming system.Each group had two independant biological repeats .


title: Microarray expression analysis in idiopathic and LRRK2-associated Parkinson's disease (PD)

city: Barcelona

first: Mario

last: Ezquerra

state: Catalonia

address: Villarroel 170

department: Neurology

country: Spain

institute: Fundacio Clinic/IDIBAPS

summary: We analysed the RNA profile of IPSC-derived dopaminergic neurons from idiophatic and genetic form (LRRK2) of Parkinson’s disease (PD). Both, idiopathic and genetic form of the disease show similar expression alterations and were merged in one whole PD group. We found 437 differentially expressed genes (DEGs) in the PD group as a whole. Up-regulated DEGs (n=254) encompassed genes involved in neural functions and transcription factor functions whereas down-regulated DEGs (n=183) affected basic homeostasis. These data point towards the presence of gene - and also protein - expression changes in DAn from PD patients which co-occur simultaneously along with DNA methylation changes.

overall_design: Number of samples analyzed: 14 iPSC-derived dopaminergic neurons . Control (C) samples, no pathological changes: SP9,   SP11   SP15  SP17. Samples from idiopathic Parkinson's Disease (IPD) patients: SP1,  SP2, SP4,  SP8, SP10, SP16. Samples from Parkinson's disease patients carriers of G2019S LRRK2 mutation (MPD): SP5,  SP6, SP12, SP13. No replicates. 30 days of cell culture.

first: Ruben

last: Fernandez-Santiago

first: Eduardo

last: Tolosa

first: Àlex

last: Sànchez-Pla

first: Jose

last: Mosquera


title: Gene expression profile of E18.5 epidermis from WT and MafB KO mice

status: Public on Nov 26 2015

city: Yokohama

first: Kohsuke

last: Kataoka

address: 1-7-29 Suehiro-cho, Tsurumi-ku

institute: Yokohama City University

summary: MafB is a member of the Maf family of bZip transcription factor and plays important roles in the developmental processes of various tissues, as well as in cell-type specific gene expression. MafB is expressed in differentiating keratinocytes in mice and is transcriptionally up-regulated upon human keratinocyte differentiation in vitro. In MafB-deficient mice, epidermal differentiation is partially impaired and the cornified layer is thinner. To gain insights into more detailed molecular mechanisms of MafB regulation of epidermal development, we performed microarray analysis of mRNAs isolated from dorsal skin epidermis of MafB-/- and wild-type mice at E18.5.

overall_design: Epidermis was separated from dorsal skin tissues of E18.5 mouse embryos (MafB-/- and WT) by Dispase (Life Technologies) treatment. Total RNA was isolated using Trizol reagent (Life Technologies), purified using an RNeasy mini kit (Qiagen), and subjected to microarray analysis.


title: PI3 Kinase and FOXO1 activity differentially control B cells in the germinal center light and dark zone

status: Public on Nov 23 2015

city: Berlin

first: Lars

last: Bullinger

address: Augustenburger Platz 1

department: Hematology, Oncology and Tumorimmunology

institute: Charité

summary: PI3K signaling and FOXO transcription factors play opposing roles at several B cell developmental stages. We show here abundant nuclear FOXO1 expression in the proliferative compartment of the germinal center (GC), its dark zone (DZ), and PI3K activity, downregulating FOXO1, in the GC light zone (LZ), where cells are selected for further differentiation. However, here FOXO1 is expressed in c-Myc+ cells destined for DZ reentry. Upon FOXO1 ablation by genetic means or induction of PI3K activity GCs become devoid of their DZ, due at least partly to the downregulation of the chemokine receptor CXCR4. While this is known to prevent proper cyclic selection of cells expressing high-affinity antibodies, the initiation of immunoglobulin switching is essentially dependent on FOXO1 activity.

overall_design: All samples were obtained from mouse germinal center (GC) B cells (Cgamma1-cre; YFP, P110*, FOXO1 f/f or PTEN f/f animals). Cells used for microarray analysis were FACS sorted cells.

first: Sandrine

last: Sander

first: Klaus

last: Rajewsky


title: GE/miRNA expression profile of Human Epicardial Adipose Tissue (EAT) and Subcutaneous Adipose Tissue (SAT) in Patients with Coronary Artery Disease (CAD) vs. Controls (CTRL) - PART 2 - miRNA

status: Public on Nov 22 2015

city: Bari

first: Antonio

last: Moschetta

address: Via Orazio Flacco, 65

institute: IRCCS Ospedale Oncologico di Bari

summary: miRNA expression profiles of Human EAT vs. SAT (CTRL & CAD). The aim of the present study was to assess a miRNA expression chart characterizing EAT vs. SAT, and CAD vs. CTRL. Results provide the information that EAT is characterized by a differential expression of different miRNA when compared to its reference tissue (SAT), and that EAT is characterized by specific miRNA expression changes in patients with CAD.

overall_design: RNA obtained from EAT & SAT of the same patients (paired samples). Comparisons: EAT vs. SAT (paired samples) & CAD vs. CTRL

first: Michele

last: Vacca

first: Andria

last: D'Orazio


title: GE/miRNA expression profile of Human Epicardial Adipose Tissue (EAT) and Subcutaneous Adipose Tissue (SAT) in Patients with Coronary Artery Disease (CAD) vs. Controls (CTRL)

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

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

overall_design: Refer to individual Series


title: ATF4 governs functional expansion of hematopoietic stem cells partially via Angptl3 in the fetal liver microenvironment (array)

status: Public on Nov 20 2015

city: Beijing

first: dan

last: liu

address: NO.1 Beichen West Road, Chaoyang District, Beijing

institute: Beijing Institute of Genomics, Chinese Academy of Sciences

summary: In this study, we demonstrated that deletion of the activating transcription factor 4 (ATF4) resulted in severely impaired HSC expansion in the fetal liver at E12.5 and E15.5. In contrast, generation of the first HSC population in the aorta-gonad-mesonephros region at E11.5 was not significantly affected. Furthermore, the HSC-supporting ability of both endothelial and stromal cells in fetal liver was significantly compromised in the absence of ATF4. Gene profiling using RNA-seq revealed down-regulated expression of a panel of cytokines in ATF4-/- stromal cells, including angiopoietin-like protein 3 (Angptl3) and vascular endothelial growth factor-A (VEGFA).

overall_design: To investigate the molecular pathways of ATF4 in the stromal cells and LSK cells in the fetal liver.

first: Tao

last: Cheng

first: Bing

last: Liu

first: Yunze

last: Zhao

first: Jie

last: Zhou

first: Dan

first: Fang

last: Dong

first: Hui

first: Weili

last: Wang


title: Expression data from the brain of Mus musculus upon intrastriatal administration of baculoviral vectors

status: Public on Nov 21 2015

city: Singapore

first: Timothy

middle: Weixin

last: Kwang

address: 46 Kim Yan Road, The Herencia #01-14/15

country: Singapore

institute: Tessa Therapeutics Pte. Ltd.

summary: Recombinant insect baculoviral vectors (BV) efficiently transduce several types of cells in the brain and can possibly be used for gene therapy for brain disorders. To verify the suitability of using these viral vectors to develop gene therapy strategies in the brain, and to evaluate our method of virus purification, we evaluated immune reactions upon acute administration of BV that were purified by ion-exchange membrane chromatography with high-speed centrifugation or high-speed centrifugation alone into the mouse brain using microarray global gene expression profiling.

overall_design: Adult male mice (Mus musculus) were administered with baculoviral vectors purified by membrane chromatography with high-speed centrifugation (MC+HS) or baculoviral vectors purified by high-speed centrifugation (HS) alone into the brain. We sought to compare the gene expression changes in the brain triggered by MC+HS-purified and HS-purified baculoviral vectors.

first: Ghayathri

last: Balasundaram


title: Hippocampal gene expression in aged and young HSD1 knockout mice

city: G20 0SP

first: Donald

last: Dunbar

address: West of Scotland Science Park

country: United Kingdom

institute: Sistemic Ltd

summary: Mice deficient in the glucocorticoid-regenerating enzyme 11β-HSD1 resist age-related spatial memory impairment. To investigate the mechanisms/pathways involved, we used microarrays to identify differentially expressed hippocampal genes that associate with cognitive ageing and 11β-HSD1. Aged wild-type mice were separated into memory-impaired and unimpaired relative to young controls according to their performance in the Y-maze. All individual aged 11β-HSD1-deficient mice showed intact spatial memory. The majority of differentially expressed hippocampal genes were increased with ageing (e.g. immune/inflammatory response genes) with no genotype differences. However, the neuronal-specific transcription factor, Npas4 and immediate early gene, Arc were reduced (relative to young) in the hippocampus of memory-impaired but not unimpaired aged wild-type or aged 11β-HSD1-deficient mice. Quantitative RT-PCR and in situ hybridization confirmed reduced Npas4 and Arc mRNA expression in memory-impaired aged wild-type mice. These findings suggest that 11β-HSD1 may contribute to the decline in Npas4 and Arc mRNA levels associated with memory impairment during ageing, and that decreased activity of synaptic plasticity pathways involving Npas4 and Arc may, in part, underlie the memory deficits seen in cognitively-impaired aged wild-type mice.

overall_design: 20 samples, 5 groups of 4 biological replicates each. Young, Wild Type animals are overall controls


title: Whole genome expression data from WT, Atf4-/-, and Cebpg-/- MEFs under normal and amino acid deprived (AAD) growth conditions

status: Public on Nov 19 2015

city: Frederick

first: Peter

middle: F

last: Johnson

state: MD

address: 1050 Boyles Street

department: Mouse Cancer Genetics Program

institute: NCI-Frederick

summary: The integrated stress response (ISR) controls cellular adaptations to nutrient deprivation, redox imbalances and ER stress. ISR genes are upregulated in stressed cells, primarily by the bZIP transcription factor ATF4 through its recruitment to cis-regulatory C/EBP:ATF response elements (CAREs) together with a dimeric partner of uncertain identity. Here we show that C/EBPγ:ATF4 heterodimers, but not C/EBPβ:ATF4 dimers, are the predominant CARE binding species in stressed cells. C/EBPγ and ATF4 associate with genomic CAREs in a mutually-dependent manner and co-regulate many ISR genes. By contrast, the C/EBP family members C/EBPβ and CHOP were largely dispensable for induction of stress genes.  Cebpg−/− MEFs proliferate poorly and exhibit oxidative stress due to reduced glutathione levels and impaired expression of several glutathione biosynthesis pathway genes. Cebpg−/− mice (C57BL/6 background) display reduced body size and microphthalmia, similar to ATF4-null animals. In addition, C/EBPγ-deficient newborns die from atelectasis and respiratory failure which can be mitigated by in utero exposure to the anti-oxidant, N-acetyl-cysteine. Cebpg−/− mice on a mixed strain background show improved viability but, upon aging, develop significantly fewer malignant solid tumors compared to WT animals. Our findings identify C/EBPγ as a novel anti-oxidant regulator and an obligatory ATF4 partner that controls redox homeostasis in normal and cancerous cells.

overall_design: WT, Atf4-/-, and Cebpg-/- MEFs (passage 3) were cultured under normal and AAD conditions.  RNA from each treatment condition was collected in triplicate for hybrization on Affymetrix Mouse Genome 430 2.0 microarrays.

first: Christopher

last: Huggins


title: cDNA microarray assays to evaluate immune responses following intracranial injection of baculoviral vectors in nonhuman primates

sample_organism:
Macaca fascicularis
Mus musculus

platform_organism:
Macaca mulatta
Mus musculus


title: Expression data from 3T3-L1 preadipocytes and 10Thalf mesenchymal stem cells

city: Akita

first: Yoshihiro

last: Matsumura

state: Akita

address: Hondo 1-1-1

department: Biochemistry and Metabolic Science

institute: Akita University Graduate School of Medicine

summary:
Bivalent H3K4me3 and H3K27me3 chromatin domains in embryonic stem cells keep active developmental regulatory genes expressed at very low levels and poised for activation. Here, we show an alternative and previously unknown bivalent modified histone signature in lineage-committed mesenchymal stem cells and preadipocytes that pairs H3K4me3 with H3K9me3 to maintain adipogenic master regulatory genes (Cebpa and Pparg) expressed at low levels yet poised for activation when differentiation is required. We show lineage-specific gene-body DNA methylation recruits H3K9 methyltransferase SETDB1 which methylates H3K9 immediately downstream of transcription start sites marked with H3K4me3 to establish the bivalent domain. At the Cebpa locus, this prevents transcription factor C/EBPβ binding, histone acetylation, and further H3K4me3 deposition and is associated with pausing of RNA polymerase II, which limits Cebpa gene expression and adipogenesis.
We used microarrays to detail the global programme of gene expression in 3T3-L1 preadipocytes and 10Th1lf mesenchymal stem cells and identified up-regulated genes upon knockdown of SETDB1, MBD1, and MCAF1.

overall_design: SETDB1, MBD1, or MCAF1 was knocked-down in 3T3-L1 preadipocytes and 10Thalf mesenchymal stem cells for RNA extraction and hybridization on Affymetrix microarrays. Small interfering RNAs (siRNA) targeting to Setdb1, Mbd1, or Mcaf1 was transfected to 3T3-L1 preadipocytes or 10Thalf mesenchymal stem cells.


title: Rb family triple knock out liver progenitor cells

status: Public on Nov 15 2015

city: Philadelphia

first: Pichai

last: Raman

state: PA

address: 3501 Civic Center Blvd

institute: Children's Hospital of Philadelphia

summary: This serie was performed on liver progenitor isolated based on their expression of the Sca1 surface marker. It contains two independent samples from Rb family deficient liver and three independent samples from control liver, all isolated 2 weeks after Tamoxifen-induced Rb family ablation. Hematopoietic (CD45, Ter119) and endothelial (CD31) markers were used as negative selection markers to exclude blood or endothelial cells from the isolated fraction.

overall_design: Each liver was digested to obtain single cell suspension. Cells were positively enriched on column for Sca1 expression and further stained with antibodies against CD45, Ter119 and Cd31. Each sample represents 20-30K cells isolated by flow cytometry and sorted directly into Trizol

first: Patrick

last: Viatour


title: Expression profile of mouse carotid body and adrenal medulla [Affymetrix]

status: Public on Nov 11 2015

city: Stanford

first: Mark

last: Krasnow

address: 279 Campus Dr

institute: Stanford School of Medicine

summary:
The carotid body is a chemoreceptor that senses decreases in blood oxygen to increase breathing in hypoxia.
To look for candidate oxygen sensors in the carotid body, we compared the gene expression of the carotid body to the adrenal medulla, a similar tissue that does not have oxygen sensitivity in adults.

overall_design: For each sample, we pooled 18 carotid bodies or 10 adrenal medullas from 10 adult mice.  Group numbers designate the same cohort of animals.

first: Andy

last: Chang

middle: A


title: Transcriptional Landscape of Cardiomyocyte Maturation

status: Public on Nov 16 2015

city: Baltimore

first: Hideki

last: Uosaki

address: 720 Rutland Ave, Ross 954

department: Division of Cardiology

institute: Johns Hopkins University

summary: Decades of progress in developmental cardiology has advanced our understanding of the early aspects of heart development, including cardiomyocyte (CM) differentiation. However, control of CM maturation which is subsequently required to generate adult myocytes, remains elusive.  Here, we analyzed over 200 microarray datasets from early embryonic to adult hearts and identified a large number of genes whose expression shifts gradually and continuously during maturation. We generated an atlas of integrated gene expression, biological pathways, transcriptional regulators, and gene regulatory networks (GRNs), which show discrete sets of key transcriptional regulators and pathways activated or suppressed during CM maturation. We developed a GRN-based program named MatStatCM that indexes CM maturation status. MatStatCM reveals that pluripotent stem cell-derived CMs mature early in culture, but are arrested at the late embryonic stage with aberrant regulation of key transcription factors. Our study provides a foundation for understanding CM maturation.

overall_design: We have analyzed >200 microarray dataset from GEO for heart development and maturation. To assess maturation status of pluripotent stem cell derived cardiomyocytes (PSC-CMs) in vitro, we differentiate PSC-CMs, cultured up to 30 days and performed microarray analysis.

last: Cahan

first: Dong

last: Lee

first: Songnan

first: Matthew

last: Miyamoto

first: Laviel

last: Fernandez

first: David

last: Kass

first: Chulan

last: Kwon


title: Density variation and MMP3 treatment of SCp2 mouse mammary epithelial cells

status: Public on Nov 17 2015

city: Jacksonville

first: Derek

middle: Charles

last: Radisky

state: Florida

address: 4500 San Pablo Road

department: Cancer Biology

institute: Mayo Clinic

summary: Response of mouse mammary epithelial cells to different cell densities and treatment with  MMP3

overall_design: Cells were plated in 35 mm dishes at 50K, 100K, or 250K (experiment A), or 25K, 50K, 100K, or 250K (Experiment B), then treated as controls or with MMP-3 for three days, then isolated for RNA.

middle: C


title: Differential gene expression in spinal cords from uninfected WT mice and infected RdRP transgenic mice (2 days post infection with Encephalomyocarditis Virus, EMCV)

status: Public on Nov 08 2015

city: Rochester

first: Meghan

middle: M

last: Painter

state: MN

address: 200 1st St SW

department: Mayo Graduate School of Medicine

summary: Previously, we reported that mice made transgenic for a picornaviral RdRP – the 3Dpol protein of Theiler’s murine encephalomyelitis virus (TMEV) – suppress infection by diverse viral families. How the picornaviral RdRP transgene exerted antiviral protection in vivo was not known. To investigate the molecular mechanism, we determined gene expression profiles in spinal cords of WT and RdRP transgenic mice prior to (baseline) and after (2 days) infection with Encephalomyocarditis Virus (EMCV).

overall_design: Spinal cords from adult age-matched WT mice were harvested prior to (baseline) viral infection and RdRP transgenic spinal cords were harvested after (2 days) infection with Encephalomyocarditis Virus (EMCV). Total RNA was isolated (Qiagen RNeasy kit) and used as a template to synthesize biotinylated cRNA which was then hybridized to the HT Mouse Genome 430 2.0 GeneChip Array (Affymetrix).

first: Eric

last: Poeschla

first: Moses

last: Rodriguez


title: Expression data from WT and Fezf2 KO mTECs

status: Public on Nov 05 2015

city: Bunkyo

first: Hiroyuki

last: Takaba

department: Immunology

institute: University of Tokyo

summary:
Fezf2 is highly and specifically expressed in mTECs in mouse thymus and Fezf2 deficiency (Fezf2 KO) in the thymus leads to autoimmunity. However, it is unclear how Fezf2 contributes to thymic gene expression.
We collected WT and Fezf2 KO mTECs by FACS, and performed microarrays to determine genes regulated by Fezf2.

overall_design: mTECs were subjected to RNA extraction (from WT or Fezf2 KO mTECs) and hybridization on Affymetrix microarrays.


title: Differential gene expression in spinal cords from WT mice during uninfected (baseline) conditions and after (2 days post) infection with Encephalomyocarditis Virus (EMCV)

overall_design: Spinal cords from adult age-matched, sex-matched WT mice were harvested prior to (baseline) and after (2 days post) EMCV viral infection. Total RNA was isolated (Qiagen RNeasy kit) and used as a template to synthesize biotinylated cRNA which was then hybridized to the HT Mouse Genome 430 2.0 GeneChip Array (Affymetrix).


title: eQTL in HBV-related liver samples

status: Public on Nov 13 2015

first: Yuanfeng

last: Li

address: No.38 shengmingyuan Road

institute: Beijing Institute of Radiation Medicine

summary: 31 non-tumor liver tissues from 31 HBV-related HCC patients

overall_design:
We performed correlation analyses between the SNPs genotypes and the mRNA expression levels to evaluate whether a SNP serves as an expression quantitative trait locus (eQTL) with putative cis regulatory effects on gene expression traits in liver tissues. The intensity of all gene array experiments were normalized together using the Robust Multiarray Averaging (RMA) method.
This submission represents mRNA expression component of study.

first: Gangqiao

last: Zhou

first: Hongxing

last: Zhang


title: Gene expression in WT and Ikaros-deficient LSK cells

status: Public on Nov 03 2015

city: Illkirch

first: Attila

last: Oravecz

address: 1 rue Laurent Fries

country: France

institute: IGBMC

summary:
The Ikaros zink finger transcription factor is a critical regulator of the hematopietic system, and plays an important role in the regulation of the development and function of several blood cell lineages.
We used microarrays to characterize how Ikaros deficieny affects global transcription in the hematopoietic stem and progenitor cells from wild-type and Ikaros mutant mice.

overall_design: lin- Sca1+ c-Kit+ (LSK) cells, that contains the hematopoietic stem cells and the multipotent progenitor cells, were sorted by FACS from the bone marrow of 6-7 weeks old WT and IkL/L mutant mice. Total RNA extracted from these cells was subjected to transcriptome analysis.

first: Philippe

last: Kastner


title: Functional genomic analysis of the impact of camelina (Camelina sativa) meal on Atlantic salmon (Salmo salar) distal intestine gene expression and physiology

city: St. John's

first: Tyler

last: Brown

state: Newfoundland

address: 1 Marine Lab Road

department: Biology

country: Canada

institute: Memorial University of Newfoundland

summary: Fish were fed a standard fish meal (FM) diet or a diet with partial replacement of FM with solvent extracted camelina meal (CM) (8%, 16% or 24% CM inclusion) during a 16-week feeding trial. A significant decrease in growth performance was seen in fish fed the CM inclusion diets. A 44k oligonucleotide array experiment was used to identify any differentially expressed transcripts in the distal intestine of the fish fed the 24% CM diet compared to the control. The expression level of these genes was validated using quantitative polymerase chain reaction, which was also used to measure transcript expression in the fish fed the 8% CM and 16% CM diets. Histopathological analysis was used to quantify any physical signs in inflammation in the distal intestine of the Atlantic salmon fed the CM-containing diets.

overall_design: Two condition experiment, 0% CM vs 24% CM, Biological replicates: 9 control replicates, 9 expermiental replicates

middle: D

first: Tiago

last: Hori

first: Xi

last: Xue

first: Chang

last: Ye

last: Anderson

last: Rise


title: Expression data from the spinal cord of wild-type C57Bl/6 mice

city: Columbus

first: Hamdy

last: Awad

state: Ohio

address: 410 W 10th Avn.

department: Anesthesiology

institute: Ohio State University

summary:
The spinal cords of mice submitted to aortic cross-clamping for 7.5 minutes present with gray matter damage and central cord edema. 60% of mice subsequently experience hindlimb and tail paralysis.
We used microarrays to detail the global programme of gene expression following aotic cross-clamping, in order to identify genes that could be responsible for edema and paralysis.

overall_design: RNAs extracted from the rostral (above T6) and caudal (below T6) part of the spinal cords of wild-type mice 24 and 48 hours following aortic cross-clamping were used for hybridization on Affymetrix microarrays. Mice submitted to sham surgery were used as controls.

first: Esmerina

last: Tili


title: Differential gene expression in spinal cords from WT and transgenic RdRP mice during uninfected (baseline) conditions

last: Painter

overall_design: Spinal cords from adult age-matched, sex-matched WT or RdRP mice were harvested prior to (baseline) viral infection. Total RNA was isolated (Qiagen RNeasy kit) and used as a template to synthesize biotinylated cRNA which was then hybridized to the HT Mouse Genome 430 2.0 GeneChip Array (Affymetrix).


title: Expression following beta-catenin stabilization in synovial sarcomagenesis

status: Public on Nov 04 2015

city: Salt Lake City

first: Kevin

middle: B

last: Jones

state: Utah

address: 2000 Circle of Hope Drive, Room 4263

department: Department of Orthopaedics

institute: University of Utah

summary: Synovial sarcoma is a deadly soft-tissue malignancy with a predilection for adolescents and young adults. Mice recapitulate synovial sarcomagenesis from expression of SS18-SSX2 in certain cells. Concomitant expression of a stabilized form of beta-catenin enhances synovial sarcomagenesis and expands the potential cells of origin.

overall_design: Mice bearing conditional expression of SS18-SSX2 from the Rosa26 locus and conditional excision of the 3rd exon of beta-catenin, each activated in the leg by Cre-recombinase expressed from an adeno-associated viral vector, formed large tumors at brief latency.

first: Mario

middle: R

last: Capecchi


title: Loss of Ezh2 promotes a midbrain-to-forebrain identity switch by direct gene derepression and Wnt-dependent regulation

status: Public on Nov 09 2015

city: Zurich

first: Martina

last: Zemke

address: Winterthurerstrassse 190

department: Institute of Anatomy

country: Switzerland

institute: University Zurich

summary:
Background:
Precise spatiotemporal control of gene expression is essential for the establishment of correct cell numbers and identities during brain development. This process involves epigenetic control mechanisms, such as those mediated by the polycomb group protein Ezh2 that catalyzes trimethylation of histone H3K27 (H3K27me3) and thereby represses gene expression.
Results:
Here we show that Ezh2 plays a crucial role in development and maintenance of the midbrain. Conditional deletion of Ezh2 in the developing midbrain resulted in decreased neural progenitor proliferation, which is associated with derepression of cell cycle inhibitors and negative regulation of Wnt/β-catenin signaling. Of note, Ezh2 ablation also promoted ectopic expression of a forebrain transcriptional program involving derepression of the forebrain determinants Foxg1 and Pax6. This was accompanied by reduced expression of midbrain markers, including Pax3 and Pax7, as a consequence of decreased Wnt/β-catenin signaling.
Conclusion:
Ezh2 is required for appropriate brain growth and for maintenance of regional identity by H3K27me3-mediated gene repression and control of canonical Wnt signaling.

overall_design: After tissue isolation from dorsal midbrains of embryonic day (E) 10.5 embryos, total RNA was isolated with the RNAeasy kit (Qiagen) and RNase-Free DNase Set (79254, Qiagen) following the manufacturer’s instructions. Isolated total RNA of E10.5 control (n=3, from 2 different litters) and Ezh2 cko (n=3, from 2 different litters) dorsal midbrains was used for microarray analysis performed at the Functional Genomics Center Zurich (FGCZ), Switzerland, using the Affymetrix A430 platform.

first: Kalina

last: Draganova

first: Annika

last: Klug

first: Anne

last: Schöler

first: Luis

last: Zurkirchen

first: Max

middle: H

last: Gay

first: Phil

last: Cheng

first: Haruhiko

last: Koseki

first: Tomas

last: Valenta

first: Dirk

last: Schübeler

first: Konrad

last: Basler

first: Lukas

last: Sommer


title: Expression data from Wild type and SIRT6 konckout Hematopoietic stem cell

status: Public on Jun 01 2016

city: hangzhou

first: Hu

last: Wang

address: wenyixi road 1378

institute: hangzhou normal university

summary:
Gene expression is tightly regulated in Hematopoietic stem cells (HSCs).  SIRT6 play a important role in HSCs function.
We used microarrays to detail the global programme of gene expression in SIRT6 KO HSC

overall_design: SIRT6 knockout HSC and Wild type HSC were selected  for RNA extraction and hybridization on Affymetrix microarrays.

first: Zhenyu

last: Ju


title: Lysosomal and phagocytic activity is increased in astrocytes during the progression of amyotrophic lateral sclerosis

status: Public on Nov 02 2015

city: Sheffield

first: Paul

middle: Roy

last: Heath

state: S. Yorks

address: SITraN, 385a Glossop Road

department: Academic Neurology Unit

institute: University of Sheffield

summary: The aim of the present study is to combine LCM and microarray analysis to study how astrocytes in the spinal cord of transgenic SOD1 G93A mice and their non-transgenic (NTg) littermates respond to stimuli determined by the presence of the human mutant protein throughout the evolution of the disease by looking at the symptomatic and late-stage disease time points.

overall_design: Astrocytes have been isolated from the spinal cord of G93A mice and non transgenic littermates at different time points and the transcription expression profile of the isolated astrocytes has been analysed

first: David

last: Baker

first: Daniel

last: Blackburn

first: Marcus

last: Keatinge

first: Dilraj

last: Sokhi

first: Paulius

last: Viskaitis

first: Laura

last: Ferraiuolo

first: Janine

last: Kirby

first: Pamela

last: Shaw


title: In vitro transcriptomic comparison of daptomycin-resistant Staphylococcus aureus

status: Public on Nov 01 2015

city: Geneva

first: FRANCOIS

last: Patrice

state: Ge 4

address: Rue Gabrielle-Perret-Gentil, 4

department: Service of Infectious Diseases

institute: Genomic Research Laboratory

summary: Mutants from SG511 and NCTC8325 (wild type isolates) resistant to daptomycin were obtained following serial passage experiments in vitro. Transcriptomic experiments showed alteration in the expression of genes involved in various pathways including general metabolism, cell wall regulon and lipid metabolism.

sample_organism: Staphylococcus aureus subsp. aureus NCTC 8325

platform_organism: Staphylococcus aureus subsp. aureus Mu50

platform_organism: Staphylococcus aureus subsp. aureus N315

platform_organism: Staphylococcus aureus subsp. aureus MRSA252

platform_organism: Staphylococcus aureus subsp. aureus MSSA476

platform_organism: Staphylococcus aureus subsp. aureus USA300

overall_design: Microarray was used to evaluate alteration in the transcriptome between wild type strains SG511 and NCTC8325 and their daptomycin resistant isolates, in antibiotic-free medium.

first: Anna

last: Muller

first: Fabian

last: Grein

first: Kathrin

last: Gries

first: Jacques

last: Schrenzel

first: Dörte

last: Becher

first: Patrice

last: Francois

first: Olga

last: Shamova

first: Tanja

last: Schneider

first: Hans-Georg

last: Sahl


title: Mouse Dendritic Cells Expression Data

status: Public on Oct 24 2015

city: Ann Arbor

first: yaping

last: sun

state: Michigan

address: 1500 E Medical Center Dr.

department: internal medicine

institute: university of michigan

summary:
Dendritic cells (DC) play a vital role in the induction of activation or tolerance of immune response.  Histone deacetylase (HDAC) inhibitors potently modulate experimental graft-vs-host disease, allograft rejection, and autoimmune diseases, partly through the regulation of dendritic cells. The molecular mechanisms underpinning their immunosuppressive effects on DCs are not well understood. The functional relevance of acetylation in DC responses remains undefined.
We used microarrays to detail the global program of gene expression in dendritic cells after treated with or without SAHA, a HDAC inhibitor utilized in clinic, to identify the upregulated and downregulated genes.

overall_design: To obtain overall gene expression profile, we extracted bone marrow cells from at least 3 mice for each experiment.  Purified (95% purity) mouse dendritic cells were treated with SAHA (500 nm for 12 hours) or control diluent, then used for RNA extraction and hybridization on Affymetrix microarrays.

first: Yaping

last: Sun

first: Pavan

last: Reddy


title: Characterization of RA839, a non-covalent small-molecule binder to Keap1 and selective activator of Nrf2 signalling

status: Public on Oct 31 2015

city: Frankfurt am Main

first: Daniel

last: Margerie

address: Industrial Park Hoechst, Building H831

department: R&D, Digital Data Sciences

institute: Sanofi-Aventis Deutschland GmbH

summary: The activation of the transcription factor NF-E2-related factor 2 (Nrf2) maintains cellular homeostasis in response to oxidative stress by the regulation of multiple cytoprotective genes. Without stressors the activity of Nrf2 is inhibited by its interaction with the kelch-like ECH-associated protein 1 (Keap1). Here, we describe RA839, a small molecule that binds non-covalently to the Nrf2-interacting kelch domain of Keap1 with a Kd of approximately 6 µM, as demonstrated by X-ray co-crystallization and isothermal titration calorimetry. Whole-genome DNA arrays showed that at 10 µM RA839 significantly regulated 105 genes in bone marrow-derived macrophages. Canonical pathway mapping of these genes revealed an activation of pathways linked with Nrf2 signalling. These pathways were also activated after the activation of Nrf2 by the silencing of Keap1 expression. RA839 regulated only two genes in Nrf2 knockout macrophages. Similar to the activation of Nrf2 by either silencing of Keap1 expression or by the reactive compound CDDO-Me, RA839 prevented the induction of both inducible nitric oxide synthase expression and nitric oxide release in response to lipopolysaccharides in macrophages. In mice RA839 acutely induced Nrf2-target gene expression in liver. RA839 is a selective inhibitor of the Keap1/Nrf2 interaction and a useful tool compound to study the biology of Nrf2.

overall_design: Gene expression profile of bone marrow derived murine macrophages (BMDM) from Nrf2+/+ or Nrf2-/- mice treated with RA838, siKeap1-1 or siKeap1-2 were compared to untreated DMSO control or siControl. Four biological replicates were used for each sample group.

first: Angelika

last: Winkel

first: Dieter

last: Schmoll


title: Expression data from three types of spermatogonial stem cells.

status: Public on Oct 30 2015

city: Seoul

first: Boyoun

last: Park

address: 50 Yonsei-ro, Seodaemun-gu

department: Systems biology

country: South Korea

institute: Yonsei University

summary: Multipotent spermatogonial stem cells (mSSCs) derived from SSCs are a potential new source of individualized pluripotent cells in regenerate medicine such as ESCs. We hypothesized that the culture-induced reprogramming of SSCs was mediated by a mechanism different from that of iPS, and was due to up-regulation of specific pluripotency-related genes during cultivation. Through a comparative analysis of expression profile data, we try to find cell reprogramming candidate factors from mouse spermatogonial stem cells. We used microarrays to analyze the gene expression profiles of culture-induced reprogramming converting unipotent spermatogonial stem cells to pluripotent spermatogonial stem cells.

overall_design: Three types of spermatogonial stem cells were mechanically collected according to morphological criteria for RNA extraction and hybridization on Affymetrix microarrays.

first: Dong

last: Lee

first: Insuk


title: Expression data from murine irf4-/- and irf4+/+ mature B cells purified by magnetic cell separation and stimulated with anti-CD40 antibodies and IL-4

city: New York

first: Ulf

last: Klein

address: 1130 St. Nicholas Avenue

department: Herbert Irving Comprehensive Cancer Center

institute: Columbia University

summary: Gene expression profiling of murine irf4-/- and irf4+/+ splenic B cells identifies genes regulated by the transcription factor IRF4 in CD40+IL-4 activated mature B cells.

overall_design: B cells from 12-week old irf4-/- and irf4+/+ littermate mice were isolated by magnetic depletion of non-B cells from splenic mononuclear cells and cultures with mitogens in vitro. RNA was isolated. Labeled cRNA was hybridized to microarrays and genes specifically expressed in irf4-/- vs. irf4+/+ samples.


title: Discrimination of SIRS from Sepsis in Critically Ill Adults

city: Seattle

first: Leo

last: McHugh

state: Washington

address: 425 pontius ave N, Suite 430

department: Bioinformatics

institute: Immunexpress Inc

summary:
Background: Systemic inflammation is a whole body reaction that can have an infection-positive (i.e. sepsis) or infection-negative origin. It is important to distinguish between septic and non-septic presentations early and reliably, because this has significant therapeutic implications for critically ill patients. We hypothesized that a molecular classifier based on a small number of RNAs expressed in peripheral blood could be discovered that would: 1) determine which patients with systemic inflammation had sepsis; 2) be robust across independent patient cohorts; 3) be insensitive to disease severity; and 4) provide diagnostic utility. The overall goal of this study was to identify and validate such a molecular classifier. Methods and Findings: We conducted an observational, non-interventional study of adult patients recruited from tertiary intensive care units (ICU). Biomarker discovery was conducted with an Australian cohort (n = 105) consisting of sepsis patients and post  -surgical patients with infection-negative systemic inflammation. Using this cohort, a four-gene classifier consisting of a combination of CEACAM4, LAMP1, PLA2G7 and PLAC8 RNA biomarkers was identified. This classifier, designated SeptiCyte® Lab, was externally validated using RT-qPCR and receiver operating characteristic (ROC) curve analysis in five cohorts (n = 345) from the Netherlands. Cohort 1 (n=59) consisted of unambiguous septic cases and infection-negative systemic inflammation controls; SeptiCyte® Lab gave an area under curve (AUC) of 0.96 (95% CI: 0.91-1.00). ROC analysis of a more heterogeneous group of patients (Cohorts 2-5; 249 patients after excluding 37 patients with infection likelihood possible) gave an AUC of 0.89 (95% CI: 0.85-0.93). Disease severity, as measured by Sequential Organ Failure Assessment (SOFA) score or the Acute Physiology and Chronic Health Evaluation (APACHE) IV score, was not a significant confounding variable. The diagnostic utility o  f SeptiCyte® Lab was evaluated by comparison to various clinical and laboratory parameters that would be available to a clinician within 24 hours of ICU admission. SeptiCyte® Lab was significantly better at differentiating sepsis from infection-negative systemic inflammation than all tested parameters, both singly and in various logistic combinations. SeptiCyte® Lab more than halved the diagnostic error rate compared to PCT in all tested cohorts or cohort combinations. Conclusions: SeptiCyte® Lab is a rapid molecular assay that may be clinically useful in the management of ICU patients with systemic inflammation.
SIRS and Sepsis ICU patients, admission samples

overall_design: Retrospective, mutli-site sutdy using retrospective physician adjudication as a comparator

first: McHugh

last: Leo

first: Yager

last: Thomas


title: Lentiviral expression of MiR-31 in CD8 T-cells.

first: Matthias

last: Stephan

state: WA

address: 1100 Fairview Ave. N.

department: Program in Immunology

institute: Fred Hutchinson Cancer Research Center

summary: Purpose: identify genes regulated by expression of miR-31 in primary mouse CD8 T-cells by exogenously expressing pre-miR-31 from the Plko.3g lentiviral vector. Cells infected with empty Plko.3g vectors were used as controls for infection.

overall_design: Control vector and miR-31 transduced CD8 T-cells with 4 independent biological replicates/condition

first: Howell

last: Moffett

first: Kai

middle: W

last: Wucherpfennig


title: Analysis of gene expression in Ig-lambda/kappa positive bone marrow wild type/TAK1-/- B cell

status: Public on Oct 22 2015

city: Yokohama

first: Hisaaki

last: Shinohara

address: 1-7-22 Suehiro-cho

institute: RIKEN IMS

summary: The activation signaling of transcription factor nuclear factor-kB (NF-kB) plays central role for immune system.  One of key kinase mediating this pathway is TAK1 in adaptive and innate immunity.  However, role of TAK1 in bone marrow B cell is still unclear. To know effects of TAK1-deletion, the gene expression of Ig-lambda/kappa positive cells were analyzed in comparison of wild type with TAK1-deficient bone marrow B cells.

overall_design: Bone marrow B cells were purified by depleting CD3+/Ter119+/CD11b+/DX5+/Gr1+ cells.Purified B Cells were stained with anti-Iglambda or kappa and sorted on a FACSAria (BD Biosciences ).  Two replicated samples were analyzed.


title: Effects of TSLP challenge on airway inflammation in naïve and OVA-sensitized mice

status: Public on Oct 11 2015

city: Nutley

first: Donavan

last: Cheng

state: NJ

address: 340 Kingsland Ave

department: Translational Research Sciences

institute: Hoffmann-LaRoche

summary: TSLP is believed to play a role in allergic diseases such as atopic dermatitis and asthma, through its activation of dendritic cells which later promote the induction of inflammatory Th2 cells. We sought to characterize the inflammatory response induced by TSLP challenge in naive and OVA-sensitized mice using gene expression profiling.

overall_design: Naïve and OVA-sensitized animals were given increasing doses of TSLP (Saline, Buffer alone, 150 ng TSLP, 500 ng TSLP and 1500 ng TSLP) and sacrificed 6 and 24 hours post-challenge. 8 animals were used for each sensitization-dose-time point combination.

middle: T

first: Palanikumar

last: Ravindran

first: John

last: Allard

first: Javad

last: Golji

first: Hans

last: Bitter

first: Christopher

last: Stevenson


title: Spatial interplay between Polycomb and Trithorax complexes controls transcriptional activity in T lymphocytes [array]

status: Public on Oct 10 2015

city: Chiba

first: Atsushi

last: Onodera

address: Chuo-ku Inohana 1-8-1

institute: Chiba University

summary: Trithorax group (TrxG) and Polycomb group (PcG) proteins are two mutually antagonistic chromatin modifying complexes, however, how they together mediate transcriptional counterregulation remains unknown.  Genome-wide analysis revealed that binding of Ezh2 and Menin, central members of the PcG and TrxG complexes, respectively, were reciprocally correlated.  Moreover, we identified a developmental change in the positioning of Ezh2 and Menin in differentiated T lymphocytes compared to embryonic stem cells.  Ezh2-binding upstream and Menin-binding downstream of the transcription start site (TSS) was frequently found at genes with higher transcriptional levels, and Ezh2-binding downstream and Menin-binding upstream was found at genes with lower expression in T lymphocytes.  Interestingly, of the Ezh2 and Menin co-occupied genes, those exhibiting occupancy at the same position displayed greatly enhanced sensitivity to loss of Ezh2.  Finally, we also found that different combinations of Ezh2 and Menin occupancy were associated with expression of specific functional gene groups important for T cell development.  Therefore, spatial cooperative gene regulation by the PcG and TrxG complexes may represent a novel mechanism regulating the transcriptional identity of differentiated cells.

overall_design: ES cells, B cells and T cells are profiled for mRNA expression

first: Damon

last: Tumes

first: Yukiko

last: Watanabe

first: Kiyoshi

last: Hirahara

last: Kaneda

first: Fumihiro

last: Sugiyama

first: Yutaka

last: Suzuki

first: Toshinori

last: Nakayama


title: Precision Cut Lung Slices:  A Novel Method for Examining Respiratory Diseases

summary: Bacterial infections and cigarette smoking have been linked to exacerbations of respiratory disease including severe asthma and chronic obstructive pulmonary disease (COPD). Epidemiological studies have also shown increased incidences of respiratory tract infections even in young smokers.  We have previously shown that cigarette smoke exacerbates the inflammatory response to influenza A virus (PLoS ONE. 2010 Oct 12;5(10): e13251) and nontypeable Haemophilus influenzae (Am J Respir Crit Care Med. 2009 Apr 15;179(8):666) infection. While it is well understood that cigarette smoke impairs respiratory host defense, little is known with respect to mechanisms driving the outcome of infection in smoke-exposed mice. In this study, we attempt to characterize the antibacterial responses of lung resident cells from smoke-exposed mice to TLR agonists and live pathogens by gene expression profiling and to compare similarities and differences of inflammatory profiles between mouse and man.

overall_design: C57BL/6 mice were exposed to room air or cigarette smoke for four days. Mice were exposed to twelve cigarettes (2R4 reference cigarettes; Tobacco and Health Research Institute, University of Kentucky), twice daily in a whole body smoke exposure system (SIU48, PROMECH LAB AB, Vintrie, Sweden). Mice were subsequently euthanized and the lungs inflated with a low-gelling agarose. 120 μm precision cut lung slices (PCLS) were generated.  PCLS from room-air and cigarette smoke exposed mice were stimulated ex vivo with TLR agonists (Pam3CSK for TLR2, LPS for TLR4), as well as live and heat-killed versions of Hemophilus Influenza and S. Pneumoniae.  Samples were collected 6h, 12h and 24h post-stimulation for gene expression profiling.

first: Carla

last: Bauer

first: Kristen

last: Lambert

first: Mario

last: Giron

first: Holly

last: Hilton

first: Martin

last: Stampfli

middle: S


title: Interferon-γ inhibition of Ebola virus infection

status: Public on Oct 20 2015

city: Iowa City

first: Thomas

last: Bair

state: IA

address: 335 EMRB

institute: University of Iowa

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

overall_design: Refer to individual Series


title: Interferon-γ inhibition of Ebola virus infection [Alveolar macrophage]

summary: Episodic Ebola virus (EBOV) outbreaks, such as the current one in West Africa, emphasize the critical need for novel antivirals against this highly pathogenic virus. Here, we demonstrate that interferon gamma (IFNγ) prevents morbidity and mortality associated with EBOV infection when administered to mice either 24 hours prior to or 2 hours following EBOV infection. Microarray studies with IFNγ-stimulated human macrophages identified novel interferon-stimulated genes (ISGs) that inhibit EBOV infection upon ectopic expression. IFNγ treatment reduced viral RNA levels in macrophages to a similar degree as cells treated with the protein synthesis inhibitor, cycloheximide, suggesting that IFNγ treatment inhibits genome replication. As IFNγ treatment robustly protects mice against EBOV infection, we propose that this FDA-approved drug may serve as a useful prophylactic or therapeutic strategy during EBOV outbreaks, contributing to the currently limited arsenal of filovirus antivirals.

overall_design: Total RNA was isolated from alveolar macrophages from healthy individuals.  All cells were treated with 50 ng/mL of M-CSF plus or minus 20 ng/mL of IFNg for 24 hours prior to infection.

first: Bethany

last: Rhein

first: Linda

last: Powers

first: Manu

last: Anantpadma

first: Yasuteru

last: Sakurai

first: Catherine

last: Miller-Hunt

first: Robert

last: Davey

first: Martha

last: Monick

first: Wendy

last: Maury


title: Interferon-γ inhibition of Ebola virus infection [Monocyte-derived macrophage]

overall_design: Total RNA was isolated from monocyte-derived macrophages (MDMs) from healthy individuals differentiated in the presence of 50 ng/mL of M-CSF for 6 days and then treated with or without 20 ng/mL of IFNg for 24 hours.


title: Correlating behavoir and molecular endpoints indentifies IFNγ-regulated genes in the dopaminergic system after modafinil administration in mouse

status: Public on Oct 15 2015

city: Braine L'Alleud

first: Andre

last: Nogueira da Costa

address: Chemin du Foriest 1

country: Belgium

institute: UCB Biopharma SPRL

summary:
The mechanisms of aciotn of modafinil continue to be poorly characterised and its potential for abuse remains controverted. The aim of this study was to further elucidate the mechanism of action of modafinil, through a potential behavioural and molecular association in the mouse. A conditioned place preference (CPP) paradigm was implemented to investigate the rewarding properties of modafinil. Whole genome expression and qRT-PCR analysis were performed on the ventral tegmental area (VTA), nucleus accumbens (NAC) and prefrontal cortex (PFC) of modafinil-treated and control animals.
We used microarrays to detail gene expression in the ventral tegmental area (VTA), nucleaus accumbens (NAC) and prefrontal cortex (PFC) of the vehicle and modafinil treated animals to profile whole genome expression in the selected brain regions.

overall_design: Individual mice underwent conditioned place preference testing in identical Contextual Place Prefernce test apparatus (Columbus Instruments, USA). One side was baclk with a smooth floor, and the other was white with a textured plastic floor, a neutal zone 4 cm in width separated the two compartments. During the pre-conditioning phase (days 1 and 2) the guillotine door was not present and the animals were able to roam the entire apparatus for thirty minutes to habituate to the conditioning boxes. Time spent in each compartment was recorded for the first fifteen minutes of testing during pre-conditioning to assess the natual preference of the animals. All animals displayed a preferance for the black compartment. Mice were randomly assigned into treatment groups. During the conditioning phase (days 3-10) the guillotine doors were closed. Mice received one injection per day, saline and treatment (modafinil or saline) on alternate days. On recieving saline injection, they were immediately confined to the initially preferred (black) compartment for thirty minutes. On drug conditioning days animals received an injection of modafinil 65 mg/kg or saline (control) and were immediately confined to the initially aversive (white) compartment for thirty minutes. On day eleven, the guillotine doors were again removed and the animals were allowed to explore the entire apparatus for thirty minutes. Time spent in each compartment for the first fifteen minutes of testing was recorded and used to calculate the post-conditioning preference of the animals.

first: Pierrette

last: De Ron

first: Sarah

last: Dremier

first: Poppy

last: Winlow

first: Andrew

last: Jenkins

first: Etienne

last: Hanon


title: Effects of intranasal infection with γMHV-68 in naïve, and control challenged mice

first: Donavan

last: Cheng

summary: To examine if differences in gene expression are evident following intranasal infection with γMHV-68 compared to naïve, and control challenged animals

overall_design: Naïve animals were infected with MHV-68 or vehicle, and sacrificed at 2h, 6h, 1 day, 4 day, 7 day, 14 day, 21 day, 35 day, 49 day and 70 day time points. Some animals were deliberately left untreated as a control. 8 biological replicates were obtained for each treatment-time point combination.

first: Palanikumar

last: Ravindran

first: John

last: Allard

first: Javad

last: Golji

first: Hans

last: Bitter

first: Christopher

last: Stevenson


title: Effects of OVA challenge in mouse model of asthma

summary: Challenge with ovalbumin antigen is a common model for asthma in mice. We sought to identify the gene expression differences in lung tissue in naïve and OVA-sensitized mice, in response to OVA challenge.

overall_design: Naïve and OVA-sensitized animals were challenged with OVA antigen and sacrificed at 0h, 2h, 6h, 24h, 48h, 72h, 96h and 168h post-challenge time points. At each time point, 8 animals were sacrificed.


title: Expression data from C3H10T1/2 mesenchymal stem cells

city: London

first: David

middle: E

last: Carter

state: ON

address: 1151 Richmond Street North

department: London Regional Genomics Centre

institute: Robarts Research Institute

summary:
BMP3 stimulates mesenchymal stem cell proliferation, but the down-stream molecular targets of BMP3 are unknown
We used microarrays to identify genes that are differentially regulated by BMP3

overall_design: C3H10T1/2 mesenchymal stem cells were treated with and without BMP3 for 6 hours, at the end of which total RNA was extracted and hybridized on Affymetrix microarrays

first: Kaiping

last: Yang


title: Expression data from E12.5 mouse embryonic heart

city: Nanjing

first: Zhongzhou

state: Jiangsu

address: 12 Xuefu Road

department: Model Animal Research Center

institute: Nanjing University

summary: We prepared RNA from mouse embryonic hearts and performed mRNA micro-array analysis to compare gene expression profiles between control and Rhau-deletion mice (E12.5), in order to understand how RHAU regulates heart development.

overall_design: Three hearts were dissected from each group of control and Rhau-deletion mice and total RNA was isolated from these hearts. In total, six RNA samples were applied for microarray analysis (Affymetrix Mouse 430 2.0 Array, Shanghai Biotechnology Co. Ltd.).

first: Junwei

last: Nie

first: Mingyang

last: Jiang


title: Characterization of chemokine and chemokine receptor expression during Pneumocystis infection in healthy and immunodeficient mice (part 3)

city: Frederick

first: Xiaojun

last: Hu

state: MD

address: 1050 Boyles St.

department: CSP

institute: SAIC_Frederick, INc

summary: In wild-type mice, expression of chemokines that are ligands for Ccr2, Cxcr3, and Cxcr2 increased at days 32 to 41 post-infection, with a return to baseline by day 75. Concomitant increases were seen in Ccr2 and Cxcr3 but not in Cxcr2 expression. Induction of these same factors also occurred in CD40-ligand and CD40 knockout mice but only at a much later time-point, during uncontrolled Pneumocystis pneumonia (PCP). Expression of CD4 Th1 markers was increased in wild-type mice during clearance of infection. Ccr2 and Cx3cr1 knockout mice cleared Pneumocystis infection with kinetics similar to wild-type mice, and all animals developed anti-Pneumocystis antibodies. Upregulation of Ccr2 and Cxcr3 and their ligands supports an important role for T helper cells and mononuclear phagocytes in the clearance of Pneumocystis infection. However, based on the current and prior studies, no single chemokine receptor appears to be critical to the clearance of Pneumocystis.

overall_design: Gene expression microarrays were from 2 samples of none exposure compared with 3 samples of 5 months exposure

first: Lisa

last: Bishop

first: Michail

last: Lionakis

first: Monica

last: Sassi

first: Philip

last: Murphy

first: Da

last: Huang

first: Brad

last: Sherman

first: Jun

first: Richard

last: Lempicki

first: Joseph

last: Kovacs


title: The single-stranded DNA binding protein Ssbp3 promotes trophoblast differentiation of mouse embryonic stem cells

status: Public on Oct 01 2015

city: Shanghai

first: Hui

last: Li

address: 320 Yue Yang Road

institute: Shanghai Jiao Tong University School of Medicine

summary: Unlimited self-renewal and developmental pluripotency are hallmarks of embryonic stem cells. Both properties are precisely controlled by the extrinsic signals and intrinsic factors and have been extensively investigated. However, factors capable of converting ES cells to extra-embryonic lineages have been poorly studied. Here we found that overexpression of Ssbp3 dramatically up-regulated trophoblast specific markers. Then we investigated the genome-wide transcriptional effect of ectopic Ssbp3 expression by comparing the whole genome expression profiles of Ssbp3-overexpressing cells with negative control cells using affymetrix microarray.Genetic analysis indicated that overexpression of Ssbp3 drives the trophoblast transcriptional program, induces the expression of early trophectoderm transcription factors such as Cdx2, Gata3 and Elf5, and activates MAPK and TGF-β pathways, which are essential for trophoblast derivation.Our findings identify Ssbp3 as a novel regulator converting ES cells into extra-embryonic trophoblast.

overall_design: The experiment contains two groups of samples, one group is Vector-expressing cells and the other group is Ssbp3-overexpressing cells. Each group contains duplicated biological samples. Vector or Ssbp3 was overexpressed for 96 hours in mouse E14T ES cells. Differentially expressed genes with a cutoff threshold of 2-fold were identified from the whole genome expression profiles of Ssbp3-overexpressing cells vs Vector-overexpressing cells using affymetrix microarray.

first: Jifeng

last: Liu


title: Characterization of chemokine and chemokine receptor expression during Pneumocystis infection in healthy and immunodeficient mice


title: A Detailed Characterization of the Dysfunctional Immunity and Abnormal Myelopoiesis Induced by Severe Shock and Trauma in the Aged

status: Public on Oct 06 2015

city: Gainesville

first: M Cecilia

last: Lopez

state: FL

address: 1376 Mowry Road

department: Molecular Genetics and Microbiology

institute: University of Florida

summary: The polytrauma (PT) murine model has unique transcriptomic responses 2 hrs, 1 day and 3 days after injury. We determined with this clinically relevant model that the increased morbidity in the elderly is secondary to a failure of bone marrow progenitors, blood neutrophils, and bronchoalveolar lavage cells to initiate and complete an 'emergency myelopoietic' response, engendering myeloid cells that fail to clear secondary infection. In addition, the elderly appear unable to effectively resolve their inflammatory response to severe injury.

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

first: Dina

last: Nacionales

first: Benjamin

last: Szpila

first: Ricardo

last: Ungaro

first: M

first: Jianyi

last: Zhang

first: Lori

last: Gentile

first: Angela

last: Cuenca

first: Erin

last: Vanzant

first: Brittany

last: Mathias

first: Jeevan

last: Jyot

first: Donevan

last: Westerveld

first: Azra

last: Bihorac

first: Anna

last: Joseph

first: Alicia

last: Mohr

first: Lizette

middle: V

last: Duckworth

first: Frederick

last: Moore

first: Henry

last: Baker

first: Christiaan

last: Leeuwenburgh

first: Lyle

last: Moldawer

first: Scott

last: Brakenridge

last: Efron


title: Expression data from murine fetal liver cells, combinations of RB1 family knockouts

first: Paul

last: Ney

state: NY

address: 310 E 67th St

institute: New York Blood Center

summary: Retinoblastoma-1 (RB1), and the RB1-related proteins p107 and p130, reside at a central node in the cell cycle regulatory network. RB1 is required for normal erythroid development in vitro, but is largely dispensable for erythropoiesis in vivo. The modest phenotype caused by RB1 deficiency in mice raises questions about redundancy within the RB1 family, and the role of RB1 in erythroid differentiation. Here we show that RB1 is the major pocket protein that regulates terminal erythroid differentiation. Erythroid cells lacking all pocket proteins exhibit the same cell cycle defects as those deficient for RB1 alone.  Further, we show that RB1 broadly represses gene expression in erythroid cells, coincident with the transition from precursor to terminally differentiated cell. RB1-repressed genes are well expressed but downregulated at the final stage of erythroid development. By merging differential and time-dependent changes in expression, we define a group of approximately 800 RB1-repressed genes. As anticipated, these genes are enriched for terms such as cell cycle and DNA metabolic process, but also for terms such as mRNA processing, chromosome organization, and ubiquitin-mediated protein catabolic pro-cess. Our results suggest that RB1-mediated repression of genes involved in noncanonical processes has a central role in terminal erythroid differentiation.

overall_design: There are 34 samples from freshly isolated E13.5-14.5 murine fetal livers. The samples represent various combinations of pocket protein deficiencies (RB1, p107, and p130).


title: A diet-sensitive epigenetic pathway links hepatic bile acid metabolism to cholesterol absorption and atherosclerosis

status: Public on Oct 03 2015

first: Zhuoxian

last: Meng

address: 210 Washtenaw Ave

institute: University of Michigan

summary:
Dietary nutrients interact with the gene networks to orchestrate adaptive responses during metabolic stress. Tissue metabolic reprogramming is frequently linked to induction of pathways with pathophysiological consequences. Here we identified Baf60a as a diet-sensitive subunit of the SWI/SNF chromatin-remodeling complexes in the liver that links the consumption of fat- and cholesterol-rich diet to elevated plasma cholesterol levels. The expression of Baf60a in the liver was elevated following western diet feeding. Hepatocyte-specific inactivation of Baf60a reduced bile acid production and intestinal cholesterol absorption, and attenuated diet-induced hypercholesterolemia and atherosclerosis in mice. At the mechanistic level, Baf60a stimulates the expression of hepatic genes involved in bile acid synthesis, modification, and transport through a CAR/Baf60a feedforward regulatory loop. Baf60a is required for the recruitment of the SWI/SNF chromatin-remodeling complexes to facilitate an activating epigenetic switch on the CAR target genes. These studies elucidate an unexpected regulatory pathway that mediates the hyperlipidemic and atherogenic effects of western diet consumption.
We used microarrays to elucidate the role of hepatic Baf60a in the regulation of lipid metabolism.

overall_design: Wild type and Baf60a Liver specific knockout (Baf60a LKO) mice were fed high-fat diet (Research Diets D12492) for 10 weeks. Livers were harvested after overnight starvation for RNA isolation and microarray hybridization using Affymetrix Mouse Genome 430 2.0 Array. Two independent pool RNA samples from WT and Baf60a LKO mouse livers were included in the study.

first: Zhuo-Xian

first: Lin

last: Wang

last: Chang

first: Jingxia

last: Sun

first: Jiangyin

last: Bao

first: Yaqiang

last: Li

first: Y

last: Chen

first: Jiandie

last: Lin


title: Repression by RB1 characterizes genes involved in the penultimate stage of erythroid differentiation


title: Gene expression profiling of B9 cells in response to two classes of BRAF inhibitors

city: Berkeley

first: Chao

last: Zhang

state: CA

address: 91 Bolivar Dr.

institute: Plexxikon Inc.

summary:
Selective RAF inhibitors including vemurafenib (PLX4032) have demonstrated clinical efficacy in mutant BRAF driven metastatic melanoma. The clinical effectiveness of RAF inhibitors depends on near complete abolition of the MAPK pathway output in tumors harboring BRAF mutations. However these compounds paradoxically activate the MAPK pathway in cells bearing oncogenic RAS or elevated upstream receptor signaling. This paradox can promote cellular proliferation and can manifest clinically with progression of secondary malignancies such as cutaneous squamous cell carcinomas (cuSCC). We have identified next generation RAF inhibitors (“paradox breakers”, e.g. PLX7904) that inhibit mutant BRAF cells without activating the MAPK pathway in cells bearing upstream activation.
In murine cuSCC B9 cells that express the same HRAS mutation prevalent in squamous tumors from patients treated with RAF inhibitors, the first-generation RAF PLX4032 stimulated in vitro and in vivo growth; by contrast the paradox breaker PLX7904 had no effect. Here we compared the gene expression changes in B9 cells treated overnight with PLX4032 and PLX7904.

overall_design: B9 cells were plated in 1 µM vemurafenib, 1 µM PLX7904 or 0.2% DMSO vehicle control and incubated for 17 hours. Cell lysates were harvested for RNA extraction and hybridization on Affymetrix

first: Elizabeth

last: Burton

first: Hoa

last: Nguyen


title: Microarray data from L-GMPs and GMPs

status: Public on Oct 02 2015

city: Stanford

first: Masayuki

last: Iwasaki

address: 265 Campus Drive

department: Pathology

institute: Stanford University School of Medicine

summary: A leukemia cell fraction highly enriched for LSCs was generated in a mouse model of AML induced by co-expression of MLL target genes Hoxa9 and Meis1.  Limit dilution transplantation analyses performed on various prospectively isolated leukemia cell subpopulations revealed that cells capable of transplanting AML to syngeneic recipient mice (the operational definition of LSCs) were highly enriched in the leukemia cell fraction displaying an immunophenotype (Lin- Sca1- c-kit+ CD16/32+ CD34+) comparable to normal GMPs, referred to as L-GMPs. For the purpose of identifying genes that are differentially expressed in LSCs, microarray expression profiling was performed on L-GMPs (from leukemic mice) and GMPs (from normal mouse BM) purified by flow cytometry.

overall_design: Microarray expression profiling was performed on L-GMPs (from leukemic mice) and GMPs (from normal mouse BM) purified by flow cytometry.

first: Michael

middle: L

last: Cleary


title: Transcriptional mechanisms of proneural factors and REST in regulating neuronal reprogramming of astrocytes

status: Public on Oct 05 2015

city: Neuherberg

first: Johannes

last: Beckers

address: Ingolstaedter Landstr. 1

department: Institute of Experimental Genetics

institute: Helmholtz Zentrum Muenchen

summary:
Reprogramming offers the possibility to study cell fate acquisitions otherwise difficult to address in vivo. By monitoring the dynamics of gene expression during direct reprogramming of astrocytes into different neuronal subtypes via the activation of Neurog2 and Ascl1, we demonstrate that these proneural factors control largely different neurogenic programs. Among the cascades induced, however, we identified a common subset of transcription factors required for both Neurog2- and Ascl1-induced reprogramming, and combinations of these factors comprising NeuroD4 were sufficient to generate functional neurons. Notably, during astrocyte maturation REST prevents Neurog2 from binding to the NeuroD4 locus that becomes then enriched with histone H4 lysine 20 tri-methylation.
As combinations of downstream targets are sufficient to induce reprogramming in Neurog2-resistant cultures, our data support a model of a temporal hierarchy in shutting off alternative fate in astrocyte differentiation.

overall_design: We performed gene expression microarray analysis on cultured postnatal astroctes from cerebral cortex, transduced with Neurog2ERT2 or Ascl1ERT2-encoding retrovirus

first: Giacomo

last: Masserdotti

first: Sébastien

last: Gillotin

first: Daniela

last: Drechsel

first: Martin

last: Irmler

first: Helle

last: Jørgensen

first: Steffen

last: Sass

first: Fabian

last: Theis

first: Bernd

last: Sutor

first: Benedikt

last: Berninger

first: François

last: Guillemot

first: Magdalena

last: Götz


title: Expression and role of Galectins 1 and 3 in the lesioned brain

summary:
Astrocytes react to brain injury in a heterogeneous manner with only a subset resuming proliferation and acquiring in vitro neural stem cell properties. In order to identify novel regulators of this astrocyte subset, we performed a genome-wide expression analysis of reactive astrocytes isolated 5 days after stab wound injury from the adult mouse cerebral cortex. The expression pattern was compared with astrocytes from normal cortex and adult neural stem cells isolated from the sub-ependymal zone (GSE18765). These comparisons revealed a set of genes up-regulated both in neurogenic neural stem cells and reactive astrocytes, including the lectins Galectin-1 and -3. These results, as well as the pattern of Galectin expression in the lesioned brain, led us to examine the functional significance of these lectins in brains of Galectin-1/3 double-knockout mice.
Following stab wound injury, astrocyte reactivity, proliferation and neurosphere formation were all found to be significantly reduced in the absence of Galectin-1/3. This phenotype could be recapitulated in vitro and was fully rescued by addition of Galectin-3, but not of Galectin-1. Staining of sections obtained from patients suffering from cavernoma further underline the significance of Galectin-3 expression in reactive astrocytes.

overall_design: We performed gene expression microarray analysis on reactive and non-reactive astrocytes from mouse cortical tissue.

first: Swetlana

last: Sirko

first: Sergio

last: Gascon

first: Sarah

last: Bek

last: Schneider

first: Stefanie

last: Ohlig

first: Leda

last: Dimou

first: Jara

last: Obermann

first: Francoise

last: Poirier

first: Jörg

last: Tonn

first: Christian

last: Schichor

last: Hauck

first: Yves

last: Barde


title: Expression data from murine fetal liver cells in culture, time course, combinations of RB1 and p107 knockouts

first: Paul

last: Ney

overall_design: There are 27 samples from E14.5 murine fetal livers grown in culture for the indicated time period. The samples represent various combinations of pocket protein deficiencies (RB1 and p107).


title: Cell cloning of Barrett's esophagus stem cell, gastric cardia stem cells and normal esophagus stem cells

city: Houston

first: Frank

last: McKeon

state: TX

address: 3455 Cullen Blvd

department: Biology and Biochemistry

institute: University of Houston

summary: Barrett’s esophagus confers significant risk of esophageal adenocarcinoma.  We have established the cloning of patient-matched stem cells of Barrett’s, gastric, and esophageal epithelium.  Barrett's esophagus stem cells (BE), gastric cardia stem cells (GC) and normal esophagus stem cells (Eso) from 12 patients were cloned (For BE: 12 patients, GC: 12 patients and Eso: 2 patients). Keratin 5 positive and Keratin 7 positive cells were cloned from human fetal esophageal epithelium. Using air liquid interface culture system, stem cells were induced to differentiate into mature epithelial structures.

overall_design: We cultured the cloned patient-matched stem cells of Barrett’s, gastric, esophageal epithelium, fetal esophagus cells (krt5 and krt7 + cells) and performed the ALI structure. Total RNA were isolated from them.   We used Affymetrix chips (HuEx-1_0-st-v2)  to hybridize 2 samples from each stem cell and ALI strucure.

first: Yusuke

last: Yamamoto

first: Xia

last: Wang

first: Florian

last: Kern

first: Ting

last: Zhang

first: Yuanyu

last: Hu

first: Wa

last: Xian


title: Cloning Barrett’s esophagus stem cells

summary: Barrett’s esophagus is a precancerous lesion that confers a significant risk of esophageal adenocarcinoma.  Strategies for selective eradication of Barrett’s have been stymied by our inability to identify the Barrett’s stem cell.  Here we employ novel technologies to clone patient-matched stem cells of Barrett’s, gastric, and esophageal epithelium.  Genomic analyses of Barrett’s stem cells reveal a patient-specific mutational spectrum ranging from low somatic variation similar to patient-matched gastric epithelial stem cells to ones marked by extensive heterozygous alteration of genes implicated in tumor suppression, epithelial planarity, and epigenetic regulation.  Transplantation of transformed Barrett’s stem cells yields tumors with hallmarks of esophageal adenocarcinoma, whereas transformed esophageal stem cells yield squamous cell carcinomas.  Thus Barrett’s develops from cells distinct from local eponymous epithelia, emerges without obvious driver mutations, and likely progresses through and from the generation of dominant clones. These findings define a stem cell target for preemptive therapies of a precancerous lesion.

overall_design: Expression data of Barret's esophagus stem cells cloned from patient biopsy


title: Identification of AUF1 target mRNAs

status: Public on Sep 30 2015

city: Lausanne

first: Sylvain

last: Pradervand

address: Genopode

department: CIG

institute: UNI Lausanne

type:
Expression profiling by array
Other

summary: Regulation of mRNA stability by RNA-protein interactions contributes significantly to quantitative aspects of gene expression. We have identified potential mRNA targets of the AU-rich element binding protein AUF1. Myc-tagged AUF1 p42 was induced in mouse NIH-3T3 cells and RNA-protein complexes isolated using anti-myc tag antibody beads. Bound mRNAs were analyzed with Affymetrix microarrays. We have identified 508 potential target mRNAs that were at least 3-fold enriched compared to control cells without myc-AUF1.  22.3% of the enriched mRNAs had an AU-rich cluster in the ARED Organism database, against 16.3% of non-enriched control mRNAs. The enrichment towards AU-rich elements was also visible by AREScore with an average value of 5.2 in the enriched mRNAs versus 4.2 in the control group. Yet, many mRNAs were enriched without a high ARE score suggesting that AUF1 has a broader binding spectrum than standard AUUUA repeats. AUF1 did not preferentially bind to unstable mRNAs. Still, some enriched mRNAs were highly unstable, as those of TNFSF11 (known as RANKL), KLF10, HES1, CCNT2, SMAD6, and BCL6. We have mapped some of the instability determinants. HES1 mRNA appeared to have a coding region determinant. Detailed analysis of the RANKL and BCL6 3’UTR revealed for both that full instability required two elements, which are conserved in evolution. In RANKL mRNA both elements are AU-rich and separated by 30 bases, while in BCL6 mRNA one is AU-rich and 60 bases from a non AU-rich element that potentially forms a stem-loop structure.

overall_design: We compared mRNAs in RNP-IPs from cell extracts with and without myc-AUF1 p42 induction

first: Afzal

last: Dogar

first: Larry

last: Richman

first: Barbara

last: Neupert

first: Alexandra

last: Paillusson

first: Otto

last: Hagenbüchle

first: Lukas

last: Kühn


title: ICI182780 effect on breast cancer cell in hypoxia

city: Oxford

first: Francesca

last: Buffa

address: The Weatherall Institute of Molecular Medicine

institute: University of Oxford

summary: The ER alpha positive breast cancer MCF7 cells were treated with ER alpha antagonist ICI182780 in normoxia and hypoxia. Extracted RNA was subject to microarray analysis. The goal of the experiment is to assess the ICI182780 effect on breast cancer cell in both normoxia and hypoxia.

overall_design: MCF7 cells were treated with 1uM of ICI182780 in normoxia and hypoxia (1% O2) for 24 hours. Extracted RNA from duplicated biological samples was subject to microarray analysis.

first: Jun

last: Yang

first: Dilair

last: Baban

first: Jiannis

last: Ragoussis

first: Adrian

last: Harris