title: Gene expression profile in the bone marrow of Ptpn6-insufficient mice with neutrophilic dermatosis-like disease (NDLD)

city: Chicago

first: Andrew

last: Nesterovitch

state: IL

address: 707 S. Wood Street, Annex Bldg, Suite 220

department: Dermatology

institute: Rush University Medical Center

summary: A total number of 1,511 probe sets in the bone marrow showed at least two-fold changes with FDR < 0.05, of which 256 probe sets had over four-fold changes. A group of 63 genes in the bone marrow of NDLD mice had more than a 4-fold change with FDR < 0.0001. From 503 genes encoding proteins with ITIM motif that binds to Ptpn6, 109 were up-regulated and 83 were down-regulated.

overall_design: Bone marrow samples were harvested from 5-week old homozygous Ptpn6-meb2/meb2 mice with NDLD and their wt littermates. Total RNA samples from the bone marrow and skin were isolated with Trizol (Life Technologies, Carlsbad, CA). The quality of the samples was tested with Agilent 2100 Bioanalyzer (Agilent Technologies, Santa Clara, CA).  An Affymetrix Mouse Genome 430 2.0 GeneChip Array (Affymetrix, Santa Clara CA) was employed for the study. All labeling reactions and hybridizations were carried out according to the standard GeneChip eukaryotic 3’ target labeling protocol using the One-cycle cDNA synthesis and in vitro transcription (IVT) labeling kit (Affymetrix). Signal normalization, background correction, additional quality control and all statistical analysis were performed with the use of Affymetrix Transcriptome Analysis Console (TAC) 2.0. Robust Multi-array Average (RMA) method was used for background correction and for the normalization of hybridization signal intensities across all collected samples.

first: Tibor

last: Glant


title: Examination of IL-12 and IL-33 or IL-12 + IL-33 induced mRNA in effector CD8 T cells

status: Public on Sep 30 2015

city: Farmington

first: Anthony

middle: T

last: Vella

state: CT

address: 263 Farmington Avenue

department: Immunology

country: USA

institute: University of Connecticut Health Center

summary: We used microarrays to detail the global program of gene expression in cytokine stimulated effector CD8 T cells.

overall_design: OT-I CD8 T cells primed with cognate SIINFEKL peptide and agonists to the costimulatory receptors CD134 and CD137 were stimulated with and without IL-12 and IL-33, and then microarray was performed.

first: Naomi

last: Tsurutani


title: Gene expression analysis of human fallopian tube stem cells and air-liquid interface differentiation

status: Public on Sep 29 2015

city: Houston

first: Frank

last: McKeon

state: TX

address: 3455 Cullen Blvd

department: Biology and Biochemistry

institute: University of Houston

summary: If the fallopian tube is the origin of serous cancer, one possible mechanism for the evolution of cancer is a dysregulation of indigenous stem cells.  We therefore set out to clone the stem cells of the human fallopian tube using methods to clone columnar epithelial stem cells such as human intestinal stem cells.  Using this method, we were able to generate clones of fallopian tube stem cells that contain many small, undifferentiated cells.  These stem cell clones show strong and consistent staining with markers of fallopian tube epithelial cells (PAX8).  We also established an air-liquid interface culture system to differentiate fallopian tube stem cell to both ciliated cells  and non-ciliated cells.

overall_design: Stem cell are cloned from human fallopian tube, and cells are differentiated in air-liquid interface culture system.  Total RNA was isolated with Picopure RNA isolation kit for stem cells and RNeasy kit for ALI samples.  We used affymetrix HuEx-1_0-st-v2 array to hybridize all samples.

first: Yusuke

last: Yamamoto

first: Gang

last: Ning

first: Brooke

last: Howitt

first: Lingyan

last: Wu

first: Yue

last: Hong

first: Christopher

middle: P

last: Crum

first: Wa

last: Xian


title: Effect of Neoadjuvant Chemoradiation on Pancreatic Adenocarcinoma

status: Public on Oct 01 2015

city: Royal Oak

first: Bryan

last: Thibodeau

state: MI

address: 3811 West 13 Mile Road

department: BioBank

institute: Beaumont Research Institute

summary:
Patients undergoing pancreatic resection at William Beaumont Hospital (Royal Oak, MI) were consented prior to surgery with local IRB oversight. Samples were collected at time of surgery and stored at -80°C according to CAP (College of American Pathologist)-accredited standard operating procedures. Disease pathology of frozen samples was validated with hematoxylin and eosin stained tissue sections from adjacently collected formalin fixed paraffin embedded tissue.
The objective of this study was to examine the gene expression patterns of pancreatic adenocarcinoma treated with neoadjuvant chemoradiotherapy compared to pancreatic adenocarcinoma that had not under gone neoadjuvant treatment. The results of this study demonstrate that neoadjuvant therapy alters the gene expression of pancreatic adenocarcinoma

overall_design: Samples from patients that receive neoadjuvant chemoradiation before surgery (n=6) were compared to samples from patients that did not receive any treatment prior to surgery (n=10). Additional comparisons to adjacent “normal” tissue were also made (n=10).

middle: J

last: Baschnagel

first: Laura

middle: E

last: Fortier

first: Timothy

last: Geddes

first: Barbara

middle: L

last: Pruetz

first: George

middle: D

last: Wilson


title: Molecular analysis of normal oviduct, STIC and invasive serous cancer

summary: High-grade serous cancer (HGSC) progresses to advanced stages without symptoms and the 5-year survival rate is a dismal 30%.   Recent studies of ovaries and fallopian tubes in patients with BRCA mutations revealed that pre-metastatic HGSC is found almost exclusively in the fallopian tube in a lesion termed “serous tubal intraepithelial carcinoma” or STIC.  We have performed laser captured microdissection (LCM) of normal oviduct, STIC and invasive serous cancer from each patient. A whole-genome transcriptome analysis comparing between normal oviduct, STIC and invasive serous cancer were performed. We demonstrated a clear molecular progression from normal to STIC, which shared the gene expression patterns with invasive serous cancer, suggesting a new set of genes as basis of novel detection and therapeutic approaches to HGSC at its earliest stage.

overall_design: Uisng frozen sections, LCM was performed to collect normal oviduct, STIC and invasive serous cancer regions from one patient. Samples were collected from 6 independent patiens. Total RNA was isolated with Picopure RNA isolation kit.  We used affymetrix HuEx-1_0-st-v2 array to hybridize  samples from 6 patients.


title: Stable inhibitory activity of regulatory T cells requires the transcription factor Helios

status: Public on Sep 15 2015

city: Boston

first: Hye-Jung

last: Kim

state: MA

address: 450 Brookline

department: Cancer Immunology and Virology

institute: Dana Farber Cancer Institute

summary: The maintenance of immune homeostasis requires regulatory T cells (Tregs). Given their intrinsic self-reactivity, Tregs must stably maintain a suppressive phenotype to avoid autoimmunity. We report that impaired expression of the transcription factor (TF) Helios by FoxP3+ CD4 and Qa-1-restricted CD8 Tregs results in defective regulatory activity and autoimmunity in mice. Helios-deficient Treg develop an unstable phenotype during inflammatory responses characterized by reduced FoxP3 expression and increased effector cytokine expression secondary to diminished activation of the STAT5 pathway. CD8 Treg also require Helios-dependent STAT5 activation for survival and to prevent terminal T cell differentiation. Definition of Helios as a key transcription factor that stabilizes regulatory T-cells in the face of inflammatory responses provides a genetic explanation for a core property of regulatory T-cells.

overall_design: We used microarrays to detail the global programs of gene expression by CD8 Treg (CD44+CD122+Ly49+) and conventional memory type of CD8 cells (CD44+CD122+Ly49-).

first: Hye

first: Taras

last: Kreslavsky

first: Harvey

last: Cantor


title: Nos3-/- iPSCs model concordant signatures of in utero cardiac pathogenesis [tissue]

status: Public on Sep 27 2015

city: Rochester

first: XING

last: LI

state: MN

address: 200 1st street SW

department: Health Sciences Research

institute: Mayo Clinic

summary: Through genome-wide transcriptional comparisons, this study interrogates the capacity of iPSCs to accurately model pathogenic signatures of structural cardiac defects. Herein, we studied the molecular etiology of structural cardiac defects in Nos3-/- mice via transcriptional analysis of stage-matched embryonic and iPSC-derived tissues. In vitro comparisons of differentiated embryoid bodies were calibrated to in utero benchmarks of health and disease. Integrated systems biology analysis of WT and Nos3-/- transcriptional profiles revealed 50% concordant expression patterns between in utero embryonic and ex vivo iPSC-derived tissue. In particular, up-regulation of glucose metabolism (p-value = 3.95x10-12) and down-regulation of fatty acid metabolism (p-value = 6.71x10-12) highlight a bioenergetic signature of early Nos3 deficiency during cardiogenesis that can be recapitulated in iPSC-derived tissues. The in vitro concordance of early Nos3-/- disease signatures supports the utility of iPSCs as a cell-autonomous model of structural heart defects. Moreover, this study supports the use of iPSCs as a platform to pinpoint initial stages of cardiac pathogenesis.

overall_design: The overall design is transcriptome comparison of heart ventricular tissues between CD1 and Nos3-/- mice. The study includes 12 samples (3 left ventricle samples and 3 right ventricle samples from wild type (WT) CD1 and Nos3-/- (B6.129P2-Nos3tm1unc/J) mice. At 14.5 days post coitum (dpc, E14.5), WT and Nos3-/- embryos were harvested from timed matings (15-30 embryos per triplicate sample). Left and right ventricular tissues (LV and RV) were microdissected and RNA was extracted with the RNeasy kit for microarray experiments.

first: Katherine

middle: A

last: Campbell

first: Xing

last: Li

first: Sherri

middle: M

last: Biendarra

first: Andre

last: Terzic

last: Nelson


title: Nos3-/- iPSCs model concordant signatures of in utero cardiac pathogenesis

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

overall_design: Refer to individual Series


title: Cytoplasmic mRNA level upon 4.5SH KD

city: Wako

first: Kentaro

last: Ishida

state: Saitama

address: Hirosawa

country: Japan

institute: RIKEN

summary:
We demonstrate that Myodonta-clade-specific 4.5S RNAH (4.5SH), an abundant nuclear noncoding RNA that is highly homologous to the retrotransposon SINE B1, controls the expression of multiple genes containing the antisense insertion of SINE B1
The depletion of endogenous 4.5SH with antisense oligonucleotides changes the subcellular distribution of these target transcripts containing the antisense SINE B1 insertions.

overall_design: To identify individual 4.5SH target asB1 genes, we performed a microarray analysis using cytoplasmic RNAs derived from control or 4.5SH-depeleted cells.


title: Sharpin controls differentiation and cytokine production of mesenchymal bone marrow cells

status: Public on Sep 07 2015

city: Hamburg

first: Thomas

last: Streichert

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

department: Institute For Clinical Chemistry / Central Laboratories

country: Germany

institute: University Medical Center Hamburg-Eppendorf

summary: The cytosolic protein Sharpin is as a component of the linear ubiquitin chain assembly complex (LUBAC), which regulates NF-κB signaling in response to specific ligands. Its inactivating mutation in Cpdm (chronic proliferative dermatitis mutation) mice causes multi-organ inflammation, yet this phenotype is not transferable into wildtype mice by hematopoietic stem cell transfer. Recent evidence demonstrated that Cpdm mice additionally display low bone mass, but the cellular and molecular causes of this phenotype remained to be established. Here we have applied non-decalcified histology together with cellular and dynamic histomorphometry to perform a thorough skeletal phenotyping of Cpdm mice. We show that Cpdm mice display trabecular and cortical osteopenia, solely explained by impaired bone formation, whereas osteoclastogenesis is unaffected. We additionally found that Cpdm mice display a severe disturbance of articular cartilage integrity in the absence of joint inflammation, supporting the concept that Sharpin-deficiency affects mesenchymal cell differentiation. Consistently, Cpdm mesenchymal cells displayed reduced osteogenic capacitiy ex vivo, yet this defect was not associated with impaired NF-κB signaling. A molecular comparison of wildtype and Cpdm bone marrow cell populations further revealed that Cpdm mesenchymal cells produce higher levels of Cxcl5 and lower levels of IL1ra. Collectively, our data demonstrate that skeletal defects of Cpdm mice are not caused by chronic inflammation, but that Sharpin is as a critical regulator of mesenchymal cell differentiation and gene expression. They additionally provide an alternative molecular explanation for the inflammatory phenotype of Cpdm mice and the absence of disease transfer by hematopoetic stem cell transplantation.

overall_design: Unsorted bone marrow cells from wildtype and Cpdm mice were cultured for 10 days in the presence of ascorbic acid and ß-glycerophosphate to induce osteogenic differentiation

first: Benjamin

last: Otto

first: Thorsten

last: Schinke


title: Expression data from mouse integration-free iPS cells

status: Public on Sep 14 2015

city: Beijing

first: Xiuying

last: Liu

address: Yard 28, Science Park Road, Changping District

country: China

institute: Changping Laboratory

summary: Reprogramming process can bring in genetic and epigenetic abnormalities, and these abnormalities can endow effect on gene expression of obtained iPSCs. We used Microarray to detect obvious gene expression differences between iPS cells ,which were induced using one episomal plasmid from C57BL/6 mouse embryonic fibroblasts, and one normal ES cell line from C57BL/6 inbred strain mice.

overall_design: iPS cells and control ES cells were selected in early passage for RNA extraction and hybridization on Affymetrix microarrays. To reduce the effect of in vitro culture, we chose iPS cells and ES cells in passage 7 to 10 for analysis.

first: Qi

last: Zhou

first: Libin

last: Wang


title: Genomic profiling reveals unique molecular alterations in hepatoblastomas and adjacent hepatocellular carcinomas in B3C3F1 mice

status: Public on Sep 01 2015

city: RTP

first: NIEHS

last: Microarray Core

state: NC

address: 111 T.W. Alexander Drive

department: DIR

institute: NIEHS

summary: The cell of origin of hepatoblastoma in humans and mice (HB) is unknown; it has been hypothesized to be a transformed hepatocyte, an oval cell, or a multipotent hepatic progenitor cell. In mice, the current dogma is that HBs arise within hepatocellular neoplasms as a result of further transformation from a neoplastic hepatocyte. However, there is little evidence in the literature to support a direct relationship between these two cell types. Furthermore, due to differences in etiology and development of hepatoblastoma between mice and humans, many have questioned the relevance of these tumors in hazard identification and risk assessment. In order to better understand the relationship between hepatocellular carcinoma and hepatoblastoma, as well as better determine the molecular similarities between mouse and human hepatoblastoma, global gene expression analysis and targeted Hras and Ctnnb1 mutation analysis were performed using concurrent hepatoblastoma, hepatocellular carcinoma, and associated normal adjacent liver (in the context of vehicle control liver) samples from a recent National Toxicology Program chronic bioassay. The data from this study provides a better understanding of the origins of hepatoblastoma in the B6C3F1 mice and the relevance of mouse hepatoblastoma to humans when considering chemical exposures of potential human cancer risk.

overall_design: Compare mouse hepatoblastoma versus adjacent hepatocellular carcinomas versus adjacent non-tumor liver and vehicle control normal liver, 6 replicates each group.

first: Mark

last: Hoenerhoff

first: Arun

middle: R

last: Pandiri


title: Wide-scale transcriptome disturbance underlies liver and kidney pathology from chronic ultra low dose Roundup exposure [kidney]

status: Public on Sep 04 2015

city: London

first: Matthew

last: Arno

state: LONDON

address: 150 Stamford Street

department: Genomics Centre

country: United Kingdom

institute: King's College London

summary: Glyphosate-based herbicides (GBH) are the major pesticides used worldwide. Converging evidence suggests that GBH residues pose a particular risk to the kidneys and liver. However, the existence of biological effects with negative health implications at low environmentally relevant doses remains unresolved. A previous investigation addressed this issue, by conducting a 2-year feeding study, which included 10 female Sprague Dawley rats administered via drinking water with 0.1 ppb of a major Roundup formulation (50 ng/L glyphosate equivalent dilution). Hepatorenal toxicities, as well as urine and blood biochemistry disturbances at the 15th month of age were observed. In an effort to obtain molecular mechanistic insight into the underlying causes of these pathologies, we have carried out a transcriptome microarray analysis of the liver and kidneys from these same animals. The expression of 4224 and 4447 genes were found to be disturbed respectively in liver and kidney (p<0.01, q<0.08, fold change >1.1). Among the 1319 genes whose expression was altered in both tissues, 3 functional categories were over-represented. First, genes involved in mRNA splicing and small nucleolar RNA were mostly upregulated, suggesting disruption of normal spliceosome activity. Electron microscopic analysis of hepatocytes confirmed nucleolar structural disruption. Second, genes controlling chromatin structure (especially histone-lysine N-methyltransferases) were mostly upregulated. Third, genes related to respiratory chain complex I and the tricarboxylic acid cycle were mostly downregulated. The transcription factor networks that can account for these disruptions were centered on CREB1, ESR1, YY1, c-Myc and Oct3/4 activity, which are known to closely cooperate in the regulation of gene expression after hormonal stimulation. The analysis of pathways and toxicity processes showed that these disturbances in gene expression were representative of fibrosis, necrosis, phospholipidosis, mitochondrial membrane dysfunction and ischemia, which correlate with the pathologies observed at an anatomical and histological level. Our results suggest that new studies incorporating testing principles from endocrinology and developmental epigenetics need to be performed to investigate potential consequences of exposure to low dose, environmental levels of GBH and glyphosate.

overall_design: Nine female rats were fed drinking water containing 0.1ppb Roundup formulation (50 ng/L glyphosate equivalent dilution). Ten control female rats were fed untreated drinking water. Samples of liver and kidney were taken for gene expression analysis.

first: Robin

last: Mesnage


title: Mouse Middle Ear Infection with NTHi

city: La Jolla

first: Nick

last: Webster

state: CA

address: 9500 Gilman Drive

department: Medicine

institute: UCSD

summary:
NTHi bacteria or saline were inoculated into the middle ears of mice.  Mice were sacrificed at various times to monitor the course of infection.
We used Mouse430_2 arrays to profile gene expression in response to bacterial infection

overall_design: RNA extracted at sacrifice

first: Nicholas

first: Allen

last: Ryan


title: Expression data from mouse embryonic fibroblasts

city: Onna

first: Toru

last: Suzuki

state: Okinawa

address: 1919-1 Tancha

institute: Okinawa Instutue of Science and Technology Graduate University

summary:
In addition to transcriptional regulation, mRNA degradation critically contributes to gene expression as shown by various biological analysis. The CCR4-NOT complex serves as a major deadenylase that initiates mRNA degradation.
We used microarrays to identify CCR4-NOT targets by searching for genes specifically stablized in the absence of CNOT3, a core subunit of the CCR4-NOT complex.

overall_design: Primary mouse embryonic fibroblasts (MEFs) were used for RNA extraction and hybridization on Affymetrix microarrays. CNOT3-knockdown MEFs were generated by Cre-mediated somatic recombination. We treated both control and CNOT-knockdown (CNOT3KD) MEFs with a transcriptional inhibitor, actinomycin D to focus on a stability of mRNAs.

first: Chisato

last: Kikuguchi


title: Expression data for MCMV-treated compared to Mock-treated Mut3 neurospheres

status: Public on Sep 28 2015

city: Columbus

first: Richard

last: Price

state: Ohio

address: 410 W 12th Ave

institute: The Ohio State University

summary: MCMV has been reported to infect neural stem cells in the subventricular zone.  These same cells have been shown to give rise to gliomas.  We wanted to test expression levels of RNA in this cell population after MCMV infection in a mouse model of glioma.

overall_design: Mut3 mice were either MCMV- or Mock-treated at perinatal day 2.  At 4-weeks-old mice were sacrificed and neurospheres from the subventricular zone were harvested.  After 4-5 passages total RNA was extracted from growing neurospheres.

first: Chang-Hyuk

last: Kwon


title: Nos3-/- iPSCs model concordant signatures of in utero cardiac pathogenesis [iPSCs]

first: XING

last: LI

overall_design: The overall design of this study is transcriptome comparison of induced pluripotent stem cells (iPSCs, D0 and D11) reprogrammed from tail-tip fibroblasts of adult male CD1 and Nos3-/- (B6.129P2-Nos3tm1unc/J) mice. The study includes 31 samples (6 D0 Nos3 -/- iPSCs, 10 D0 control iPSCs, 6 D11 Nos3 -/- differentiated embryoid bodies (EBs), 9 control D11 differentiated EBs).

first: Katherine

last: Campbell

first: Xing

last: Li

first: Sherri

last: Biendarra

first: Andre

last: Terzic

first: Timothy

last: Nelson


title: Dysregulation of the Transforming Growth Factor Beta Pathway in Induced Pluripotent Stem Cells Generated from Patients with Diamond Blackfan Anemia [HuEx-1_0]

status: Public on Aug 31 2015

city: Philadelphia

first: Jingping

last: Ge

state: PA

address: 3615 CivicCenter Blvd, ARC 303

department: Pediatrics

institute: Children's Hospital of Philadelphia

summary: Diamond Blackfan Anemia (DBA) is an inherited bone marrow failure syndrome with clinical features of red cell aplasia and variable developmental abnormalities. Most affected patients have heterozygous loss of function mutations in ribosomal protein genes but the pathogenic mechanism is still unknown. We generated induced pluripotent stem cells from DBA patients carrying RPS19 or RPL5 mutations. Transcriptome analysis revealed the striking dysregulation of the transforming growth factor beta signaling pathway in DBA lines. Expression of TGF beta target genes, such as TGFBI, BAMBI, COL3A1 and SERPINE1 was significantly increased in the DBA iPSCs. We quantified intermediates in canonical and non-canonical TGF beta pathways and observed a significant increase in the levels of the non-canonical pathway mediator p-JNK in the DBA iPSCs. Moreover, when the mutant cells were corrected by ectopic expression of WT RPS19 or RPL5, levels of p-JNK returned to normal. Surprisingly, nuclear levels of SMAD4, a mediator of canonical TGF beta signaling, were decreased in DBA cells due to increased proteolytic turnover. We also observed the up-regulation of TGF beta 1R, TGF beta 2, CDKN1A and SERPINE1 mRNA, and the significant decrease of GATA1 mRNA in the primitive multilineage progenitors. In summary our observations identify for the first time a dysregulation of the TGF beta pathway in the pathobiology of DBA.

overall_design: 6 Total human iPS samples were analyzed, including 2 wild type samples, 2 DBA samples with a RPS19 mutation, and 2 DBA samples with a RPL5 mutation. We generated the following pairwise comparisons using Partek Softare : RPS19 <WT; RPL5<WT. Genes with an FDR≤5% and a fold-change ≥2 were selected.

first: Marisa

last: Apicella

first: Jason

last: Mills

first: Loïc

last: Garçon

first: Deborah

last: French

first: Mitchell

last: Weiss

first: Monica

last: Bessler

first: Philip

last: Mason


title: Dysregulation of the Transforming Growth Factor Beta Pathway in Induced Pluripotent Stem Cells Generated from Patients with Diamond Blackfan Anemia


title: Expression data from isogenic Pten WT or KO mouse T-ALLs treated with DBZ or DMSO

city: New York

first: Alberto

last: Ambesi-Impiombato

state: NY

address: 1130 St. Nicholas Avenue

department: ICG

institute: Columbia University

summary:
To investigate the underlying mechanisms mediating resistance to NOTCH inhibition in Pten-null T-ALL tumor cells we performed gene expression profiling of isogenic Pten-positive and Pten-deleted leukemia lymphoblasts after acute treatment with DBZ in vivo.
This analysis revealed that, while direct NOTCH1 target genes (such as Hes1, Dtx1, PtcrA, HeyL and Notch3) are effectively downregulated in both Pten-positive and Pten-deleted tumors, genetic ablation of Pten elicits a global reversal of much of the transcriptional effects of NOTCH inhibition.

overall_design: We performed microarray gene expression analysis of GSI treatment in isogenic Pten KO or WT NOTCH1 induced leukemias

first: Daniel

last: Herranz

first: Jessica

last: Sudderth

first: Marta

last: Sánchez-Martín

first: Laura

last: Belver

first: Valeria

last: Tosello

first: Luyao

last: Xu

first: Agnieszka

last: Wendorff

first: Mireia

last: Castillo

first: J

last: Haydu

first: Javier

last: Márquez

first: José

last: Matés

first: Andrew

last: Kung

first: Stephen

last: Rayport

first: Carlos

last: Cordon-Cardo

first: Ralph

last: DeBerardinis

first: Adolfo

last: Ferrando


title: Molecular mechanisms of HIV-1 permissiveness in CCR4+CCR6+ Th17 cells

status: Public on Aug 30 2015

city: Montréal

first: Jean-Philippe

last: Goulet

state: Québec

address: C.P. 6128, succursale Centre-ville

country: Canada

institute: Université de Montréal

summary:
We previously reported that CCR4+CCR6+Th17 cells are permissive to HIV, while CXCR3+CCR6- Th1 cells are relatively resistant. To identify molecular mechanisms underlying these differences, we performed a genome-wide transcriptional profiling in CXCR3+CCR6-Th1, CCR4+CCR6-Th2, CCR4+CCR6+Th17, and CXCR3+CCR6+Th1Th17 upon TCR triggering.
Transcriptional differences between Th17 and Th1 were the most remarkable. HIV-DNA integration was highly efficient in Th17 versus Th1 upon exposure to both wild-type and VSV-G-pseudotyped HIV, indicative that post-entry mechanisms contribute to HIV permissiveness.

overall_design: 4 cell populations from up to 5 donors for a total of 19 samples.

first: Aurélie

last: Cleret-Buhot

first: Yuwei

last: Zhang

first: Delphine

last: Planas

first: Patricia

last: Monteiro

first: Julia

last: Niessl

first: Annie

last: Gosselin

first: Vanessa

middle: S

last: Wacleche

first: Mohammad-Ali

last: Jenabian

first: Jean-Pierre

last: Routy

first: Elias

middle: K

last: Haddad

first: Rafick-Pierre

last: Sékaly

first: Petronela

last: Ancuta


title: Expression data from isogenic Pten WT or KO mouse T-ALLs

first: Alberto

last: Ambesi-Impiombato


title: UG26-1B6 stroma-derived factors regulate hematopoietic stem cell maintenance

status: Public on Sep 16 2015

city: Munich

first: Robert

last: Oostendorp

state: Bavaria

address: Trogerstrasse 32

department: Klinikum Rechts der Isar Technische Universität München

institute: III. Medizinische Klinik und Poliklinik

summary:
Hematopoietic stem cell (HSC) are regulated by their ’niche’, which limits activation of HSCs, to ensure their maintenance and self-renewal.
To dissect the interactions involved during rapid activation in response to stress, we used cell co-culture as a model. Here, we studied gene expression changes of UG26-1B6 stromal cells in response to the presence of Lineage- Sca-1+ Kit+ (LSKs).

overall_design: UG26-1B6 stromal cells were used in a total of 5 conditions (before co-culture (d0), after one (d1; 24 h), two (d2) and three (d3) days of co-culture with Lineage- Sca-1+ Kit+ (LSKs), after one (d1; 24 h) day of culture medium change (control)) with 2-3 technical replicates per condition.

first: Baiba

last: Vilne

first: Olivia

last: Prazeres da Costa

first: Christian

last: Peschel


title: Pharmacology of PPAR isoform agonists on mouse

city: Dundee

first: Runxuan

state: Angus

address: Errol Road, Invergowrie

department: Information and Computational Sciences

institute: The James Hutton Institute

summary: Transcriptional consequences of pharmacologic PPAR a, d, & g agonist administration in murine liver, heart, kidney, and skeletal muscle

overall_design: Oral dosing of mice with GW501516, Rosiglitzone and WY16453 over 4, 8, & 15 days

first: Ruth

last: Stephen

first: Ross

last: Haggart

first: Stephen

last: McGuinness

first: Lucky

last: Pandey

first: Gino

last: Miele

first: Daniel

last: Crowther


title: Expression data from control and Smith-Lemli-Opitz syndrome patient-derived iPS cells - comparison of cholesterol deficient and cholesterol rich culture

status: Public on Sep 18 2015

city: Sioux Falls

first: Kevin

last: Francis

state: SD

department: Cellular Therapies

institute: Sanford Research

summary:
7-dehydrocholesterol reductase catalyzes the reduction of 7-dehydrocholesterol to cholesterol.  In Smith-Lemli-Opitz syndrome, mutations in DHCR7 prevents this conversion.  We have found iPS cells derived from SLOS patients exhibit accelerated differentiation under cholesterol poor conditions.
In this dataset, we include expression data obtained from comparision of a control iPS cell line (BJ) and a SLOS iPS cell line (A2). Cell line gene expression was compared in cholesterol rich conditions where the SLOS phenotype is suppressed. Cholesterol deficient culture of control and SLOS iPS cells demonstrated enhanced differentiation of SLOS cells over 7 days. These data are used to obtain 308 genes that are differentially expressed upon cholesterol deficient culture.
time-course expression data obtained from control and SLOS patient iPS cells after transfer from cholesterol rich to cholesterol deficient culture.

overall_design: 48 total RNA samples were isolated and hybridized on Affymetrix arrays. We generated the following pairwise comparisons using Partek: BJ 0hr vs A2 0hr; BJ 2Day vs A2 2Day; BJ 3Day vs A2 3Day; BJ 4Day vs A2 4Day; BJ 5Day vs A2 5Day; BJ 7Day vs A2 7Day. Genes with an FDR≤10% and a fold-change ≥3 were identified as significantly different. We also performed pairwise comparison of BJ and A2 samples within each cell line between subsequent isolations (i.e. BJ 0hr vs BJ 2Day; A2 3Day vs A2 4Day; etc.)

first: Forbes

last: Porter


title: Arid1a is essential for endometrial function during early pregnancy

status: Public on Aug 20 2015

city: Grand Rapids

first: Jae-Wook

last: Jeong

address: 333 Bostwick Avenue NE

department: Department of Obstetrics, Gynecology & Reproductive Biology

institute: Michigan State University

summary:
Arid1a has a critical role for modulating epithelial proliferation which is a critical requisite for fertility
We used microarrays for detail the mechanism underlying Arid1a loss during early pregnancy.

overall_design: Uteri of Arid1a f/f and Arid1a d/d mice were selected at 3.5 dpc for RNA extraction and hybridization on Affymetrix microarrays.

first: Tae

last: Kim


title: Autism-like syndrome is induced in mice by pharmacological suppression of BET proteins

status: Public on Sep 09 2015

first: Josefa

last: Sullivan

address: 1425 Madison Ave

department: Neuroscience

institute: Icahn School of Medicine at Mount Sinai

summary: Studies investigating the causes of autism spectrum disorder (ASD) point to genetic as well as epigenetic mechanisms of the disease. Identification of epigenetic processes that contribute to ASD development and progression is of major importance and may lead to the development of novel therapeutic strategies. Here we identify the bromodomain and extra-terminal domain containing transcriptional regulators (BETs) as epigenetic drivers of an ASD-like disorder in mice. We found that the pharmacological suppression of the BET proteins by a novel, highly selective and brain-permeable inhibitor, I-BET858, leads to selective suppression of neuronal gene expression followed by the development of an autism-like syndrome in mice. Many of the I-BET858 affected genes have been linked to ASD in humans thus suggesting the key role of the BET-controlled gene network in ASD. Our studies also suggest that environmental factors controlling BET proteins or their target genes may contribute to the epigenetic mechanism of ASD.

overall_design: There are 24 total samples. There are two timepoints, 2 and 12 hours. Triplicates were performed for each treatment. Control samples were prepared by treating with DMSO for each of the timepoints.

first: Ana

last: Badimon

first: Uwe

last: Schaefer

first: Pinar

last: Ayata

first: James

last: Gray

first: Chun

middle: W

last: Chung

first: Melanie

last: von Schimmelmann

first: Fan

last: Zhang

first: Neil

last: Garton

first: Nicholas

last: Smithers

first: Huw

last: Lewis

first: Alexander

last: Tarakhovsky

first: Rab

last: Prinjha

first: Anne


title: Wide-scale transcriptome disturbance underlies liver and kidney pathology from chronic ultra low dose Roundup exposure [liver]

first: Matthew

last: Arno

overall_design: Ten female rats were fed drinking water containing 0.1ppb Roundup formulation (50 ng/L glyphosate equivalent dilution). Ten control female rats were fed untreated drinking water. Samples of liver and kidney were taken for gene expression analysis.

first: Robin

last: Mesnage


title: Wide-scale transcriptome disturbance underlies liver and kidney pathology from chronic ultra low dose Roundup exposure

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

overall_design: Refer to individual Series


title: Expression data from mouse myogenic differentiation and ectopic MeCP2

status: Public on Aug 15 2015

city: Darmstadt

first: M. Cristina

last: Cardoso

address: Schnittspahnstr. 10

department: Biology

institute: Technische Universität

summary:
The methyl-cytosine binding protein 2 (MeCP2) is a reader of epigenetic DNA methylation marks and necessary and sufficient to reorganize 3D heterochromatin structure during cellular differentiation, e.g., myogenesis. In addition to global expression profile changes, myogenic differentiation is accompanied by 3D-heterochromatin reorganization that is dependent on MeCP2. MeCP2 is enriched at pericentric heterochromatin foci (chromocenters). During myogenesis, the total heterochromatin foci number per nucleus decreases while foci volumes and MeCP2 protein levels increase. Ectopic MeCP2 is able to mimic similar heterochromatin restructuring in the absence of differentiation.
We compared expression profile changes during myogenic differentiation to changes related to MeCP2-induced heterochromatin reorganization in the absence of differentiation. We used the Affymetrix 430.2 microarray system to study the expression profile changes during myogenic differentiation (myotubes vs myoblast) and MeCP2 related expression changes in transiently transfected myoblasts (high vs. low MeCP2 protein levels) in five independent experiments for each condition.

overall_design: To obtain expression profile changes during myogenic differentiation, five biological replicas of undifferentiated Pmi 28 myoblasts (MB) and in vitro differentiated Pmi 28 myotubes (MT) were cultured as described elsewhere. To obtain MeCP2 dependent and differentiation independent expression profile changes, five biological replica of undifferentiated Pmi 28 myoblasts were transiently transfected with MeCP2-YFP. Subsequently, transfected cells were FACSorted to generate MeCP2-high (R4) and -low (R5) level fractions. Total RNA was prepared for each sample out of cell pellets containing 6.5x10exp5 to 1.7x10exp6 cells and further processed according to the GeneChip Expression Analysis Technical Manual by Affymetrix and hybridized to Affymetrix 430.2 microarrays.

first: K

last: Jost

first: Bianca

last: Bertulat

last: Rapp

first: Alessandro

last: Brero

first: Tanja

last: Hardt

first: Petra

last: Domaing

first: Claudia

last: Gösele

first: Herbert

last: Schulz

first: Norbert

last: Hübner

first: M

middle: C


title: Infectious hematopoietic necrosis virus (IHNV) persistence in Sockeye Salmon: effect on brain transcriptome and response to the viral mimic poly(I:C)

status: Public on Aug 10 2015

city: Victoria

first: Ben

middle: F

last: Koop

state: BC

address: PO Box 3020 STN CSC

institute: The University of Victoria

summary: To characterise the transcriptional response in brain of Sockeye Salmon (Oncorhynchus nerka) that were persistently infected with infectious hematopoietic necrosis virus (IHNV) and to determine whether carrying the IHNV affects the ability to respond to other immunological challenges we compared the brain transcriptome of IHNV carriers, IHNV-negative survivors, and naïve Sockeye Salmon that were never exposed to IHNV. In addition we determined the transcriptional changes among carriers, survivors and naïve fish in their response to the viral mimic polyriboinosinic polyribocytidylic acid (poly(I:C)), using the cGRASP 44K salmon oligoarray.

overall_design: Fish that survived an immersion challenge with IHNV and time-matched control (naïve) fish that were never exposed to IHNV were reassigned into 2 tanks each at 271 days post challenge (dpc). One group each of the challenged and naïve fish received an intraperitoneal injection of poly(I:C). For controls, a group each of challenged and naïve fish were not injected. Brain tissues were sampled from each tank at 3 (274 dpc), 7 (278 dpc) and 10 (281 dpc) days after poly(I:C) injection. Based on the presence of IHNV in brain fish were assigned into “carriers” and “survivors”, i.e. fish with detectable and undetectable levels of IHNV, respectively. For transcriptomic profiling brain samples were analysed from naïve (n = 7), survivors (n = 7), and carriers (n = 5), as well as poly(I:C)-injected naïve (n = 7), poly(I:C)-injected survivors (n = 7), and poly(I:C)-injected carriers (n = 2). All analysed brain samples were collected 274 dpc (i.e. 3 d after poly(I:C) injection) with the exception of two carriers that were collected 278 dpc. The smaller sample size for carriers was a result of the few individuals that survived the exposure that ended up carrying the virus.

first: Anita

last: Mueller

middle: G

last: Sutherland

first: Stewart

last: Johnson

first: Kyle

last: Garver


title: A Long Non-coding RNA, LncMyoD, Regulates Skeletal Muscle Differentiation by Blocking IMP2-mediated mRNA Translation

status: Public on Aug 11 2015

city: Cambrdige

first: Yunyu

last: Zhang

address: 22 Windsor Ave

institute: Novartis Institute for Biomedical Research

summary:
Increasing evidence suggests that Long non-coding RNAs (LncRNAs) represent a new class of regulators of stem cells.  However, the roles of LncRNAs in stem cell maintenance and myogenesis remain largely unexamined. For this study, hundreds of novel intergenic LncRNAs were identified that are expressed in myoblasts and regulated during differentiation. One of these LncRNAs, termed LncMyoD, is encoded next to the Myod gene and is directly activated by MyoD during myoblast differentiation.  Knockdown of LncMyoD strongly inhibits terminal muscle differentiation largely due to a failure to exit the cell cycle.  LncMyoD directly binds to IGF2-mRNA-binding-protein 2 (IMP2) and negatively regulates IMP2-mediated translation of proliferation genes such as N-Ras and c-Myc. While the RNA sequence of LncMyoD is not well-conserved between human and mouse, its locus, gene structure and function is preserved.  The MyoD-LncMyoD-IMP2 pathway elucidates a mechanism as to how MyoD blocks proliferation to create a permissive state for differentiation.
In order to perform an unbiased search for downstream signaling pathways perturbed by LncMyodD downregulation, microarrays were performed on myoblasts treated with control vs LncMyoD shRNAs.

overall_design: Total RNA was extracted using the TRIzol reagent (Invitrogen) and purified with Qiagen RNeasy separation columns (Qiagen) from myoblasts treated with control vs. LncMyoD shRNA. First-strand cDNA was synthesized and hybridized to GeneChip Mouse Genome 430 2.0 Array (Affymetrix).

first: Chenguan

last: Gong

first: Zhizhong

last: Li

first: Krishnan

last: Ramanujan

first: Ieuan

last: Clay

first: Sophie

last: Brachat

first: David

last: Glass


title: Influence of muscle activity on paralyzed muscle

city: Iowa City

first: Richard

last: Shields

address: 1-252 Medical Education Building

institute: The University of Iowa

summary: We investigated the short and long term effects of electrically induced exercise on mRNA expression of human paralyzed muscle. We developed an exercise dose that activated the muscle for 0.6% of the day. The short term effects were assessed 3 hours after a single dose of exercise, while the long term effects were assessed after training 5 days per week for at least one year (adherence 81%). A single dose of electrical stimulation increased the mRNA expression of transcriptional, translational, and enzyme regulators of metabolism important to shift muscle toward an oxidative phenotype (PGC-1a, NR4A3, IFRD1, ABRA, PDK4). However, chronic training increased the mRNA expression of specific metabolic pathway genes (BRP44, BRP44L, SDHB, ACADVL), mitochondrial fission and fusion genes (MFF, MFN1, MFN2), and slow muscle fiber genes (MYH6, MYH7, MYL3, MYL2).Furthermore, regulating these same pathways may be critical to developing efficient activity protocols to reduce the prevalence of diabetes in people with longstanding paralysis from SCI.

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

first: Michael

last: Petrie

first: Manish

last: Suneja

first: Elizabeth

last: Faidley


title: Differences in the Transcriptional Response to Fulvestrant and Estrogen Deprivation in ER-Positive Breast Cancer

status: Public on Aug 07 2015

first: Alice

last: Gao

state: London

address: 237 Fulham Road

department: Breast Cancer Now

institute: The Institute of Cancer Research

summary: Aromatase inhibitors are first-line postmenopausal agents for estrogen receptor alpha (ERa)-positive breast cancer. However, there is considerable response heterogeneity and women frequently relapse. Estrogen deprivation does not completely arrest ERa activity, and transactivation of the unliganded receptor may continue through cross-talk with growth factor pathways. In contrast with aromatase inhibitors, the selective ER downregulator fulvestrant also abrogates ligand-independent ERa activity. The benefit of fulvestrant as an alternative, combination, or sequential therapy to aromatase inhibitor has been reported, but molecular mechanisms underpinning its relative efficacy remain unclear and biomarkers for patient selection are lacking. This study demonstrates, for the first time, that the overall transcriptional response to fulvestrant is of greater magnitude than estrogen deprivation, consistent with its clinical efficacy and more complete blockade of estrogenic signaling. Using a robust integrative approach, we identify a subset of genes differentially affected by fulvestrant that comprises distinct biologic networks, correlates with antiproliferative response, and has potential utility as predictive biomarkers for fulvestrant.

overall_design:
Global gene expression profiles from ERα-positive breast carcinomas before and during presurgical treatment with fulvestrant (n = 38) or anastrozole (n = 81), and corresponding in vitro models, were compared. Transcripts responding differently to fulvestrant and estrogen deprivation were identified and integrated using Gene Ontology, pathway and network analyses to evaluate their potential significance.
---------------------------------
This represents the data for fulvestrant only

first: Qiong

first: Lesley

last: Martin


title: Direct reprogramming of mouse fibroblasts into cardiomyocytes with chemical cocktails

status: Public on Aug 23 2015

city: Shanghai

first: Yanbin

last: Fu

address: No.1239, SiPing Road

institute: Tongji University

summary: The direct conversion, or trans-differentiation, of non-cardiac cells into cardiomyocytes by forced expression of transcription factors and microRNAs provide promising ways of cardiac regeneration. However, genetic manipulations are still not desirable in real clinical applications. we report the generation of automatically beating cardiomyocyte-like cells from mouse fibroblasts with only chemical cocktails. These chemical-induced cardiomyocyte-like cells (CiCMs) express cardiomyocyte-specific markers, exhibit sarcomeric organization, and possess typical cardiac calcium flux and electrophysiological features. Microarray-bassed gene expression patterns of Mouse embryonic fibroblasts (MEFs), CiCMs, and cardiomyocytes(CMs) indicated a clear transition from dividing MEFs to differentiated cardiomyocyte-like state in CiCM samples.

overall_design: Mouse embryonic fibroblasts were treated with a small-molecule combination CRFVPT (10 μM CHIR99021 (C); 10 μM RepSox (R); 50 μM Forskolin (F); 0.5 mM VPA (V); 5 μM Parnate, (P); 1 μM TTNPB (T)) to induce transdifferentiation to chemical-induced cardiomyocyte-like cells. CiCMs beating clusters were picked at day 24 for analysis. MEFs were isolated from mouse embryos, and CMs were isolated from mouse hearts. Total RNA of MEFs, CiCMs and CMs were extracted and hybridization on Affymetrix microarrays.

first: Y

first: C

last: Huang

first: X

last: Xu

first: H

last: Gu

last: Ye

last: Jiang

first: Z

last: Qiu

last: Xie


title: Expression data of CNS T cells during EAE

status: Public on Aug 25 2015

city: Kodaira

first: Shinji

last: Oki

state: Tokyo

address: 4-1-1 Ogawa-Higashi

department: Department of Immunology

institute: National Institute of Neuroscience, NCNP

summary:
In the absence of NR4A2 in T cells mice do not develop early acute EAE, but only a late chronic disease.  We examined the mechanism by which NR4A2 can control the pathogencity of T cells in CNS autoimmune disease.
To determine how NR4A2 is involved is involved in T cell pathology, we examined expression profiles of T cells during early and late diease in the presence or genetic CD4-specific absence of NR4A2.

overall_design: T cells infiltrating CNS tissues were isolated at peal acute EAE (D18) or during late,chronic EAE (D32).  RNA expression was then analysed by genechip to determine the influence of NR4A2 in T cells on these disease stages

first: Ben

last: Raveney

first: Takashi

last: Yamamura


title: Gene expression profiling of the prostate biopsy samples from cancer and adjacent normal tissues of European American prostate cancer patients

city: Washington

first: Bi-Dar

last: Wang

state: DC

address: 2300 I street, NW

department: Pharmacology and Physiology

institute: The George Washington University Medical Center

summary: Prostate cancer (PCa) tends to be more aggressive and lethal in African Americans (AA) compared to European Americans (EA). To further understand the biological factors accounting for the PCa disparities observed in AA and EA patients, we performed gene profiling analysis using Affymetrix human exon 1.0 ST arrays to identify the differentially expressed genes in EA PCa vs. EA normal.

overall_design: 30 prostate biopsy specimens (tumor and adjacent normal tissues) were collected from 15 European American prostate cancer patients. RNA samples, purified from the collected biopy specimens, were process and applied to Affymetrix human exon ST 1.0 arrays. Array data was normalized, batch-corrected and analyzed (2-way ANOVA) using Partek Genomics Suite program.

first: Norman

last: Lee


title: Expression data from The human glioblastoma cell culture resource: validated cell models representing all molecular subtypes (exon)

city: Uppsala

first: Sven

last: Nelander

address: Rudbecklab

country: Sweden

institute: Uppsala Universitet

summary: To meet the present shortage of relevant GBM cell (GC) lines we developed a library of annotated and validated cell lines derived from surgical samples of GBM patients, maintained under conditions to preserve GSC characteristics. This collection, which we call the Human Glioblastoma Cell Culture (HGCC) resource, consists of a biobank of GC lines and an associated database containing high-resolution molecular data.

overall_design: Total RNA extracted from GC lines using the RNeasy Mini kit (Qiagen) was labeled and hybridized on Affymetrix GeneChip Human Exon 1.0 ST arrays.  Expression levels were RMA-normalized employing the Affymetrix Expression Console software.

first: Lene

last: Uhrbom


title: Gene expression profiling of the prostate biopsy samples (cancer and adjacent normal tissues) from African American prostate cancer patients

summary: Prostate cancer (PCa) tends to be more aggressive and lethal in African Americans (AA) compared to European Americans (EA). To further understand the biological factors accounting for the PCa disparities observed in AA and EA patients, we performed gene profiling using Affymetrix human exon 1.0 ST arrays to identify the differentially expressed genes beween AA cancer and patient matched normal tissues.

overall_design: 40 prostate biopsy specimens (tumor and adjacent normal tissues) were collected from 20 African American prostate cancer patients. RNA samples, purified from the collected biopy specimens, were process and applied to Affymetrix human exon ST 1.0 arrays. Array data was normalized, batch-corrected and analyzed (2-way ANOVA) using Partek Genomics Suite program.


title: Gene expression in CD8+ T cells derived from Nrdp1+/+ and Nrdp1-/- mice

status: Public on Aug 03 2015

first: Taoyong

last: Chen

address: 800 Xiangyin Road

institute: Second Military Medical University

summary: The purpose of this study was to determine which genes are differentially regulated by the E3 ligase Nrdp1 in CD8+ T cells after treatments with anti-CD3/CD28 Abs. The results demonstrate increased induction of cytotoxicity-associated genes in Nrdp1-/- mice than in Nrdp1+/+ mice after activation. Thus Nrdp1 may be involved in the regulation of TCR signaling.

overall_design: Naive CD8+ T cells derived spleens of Nrdp1+/+ and Nrdp1-/- mice  were either untreated or treated with immobilized anti-CD3 (5 μg/ml) and soluble anti-CD28 (1 μg/ml) Abs for 4h or 8h. Equal amounts of RNA were assayed for gene expression using Affymetrix mouse 430 2.0 arrays.

first: Mingjin

last: Yang

first: Zhou

last: Yu

first: Xuelian

last: Li

first: Xuetao

last: Cao


title: Dietary selenium levels affect selenoprotein expression and support the interferon-γ and IL-6 immune response pathways in mice [microarray]

status: Public on Aug 06 2015

city: Salt Lake City

first: Michael

last: Howard

state: UT

department: Human Genetics

institute: University of Utah

summary: Mice were fed Se-deficient or Se-adequate diets for 6 weeks. Liver and lung tissue were harvested and processed for RNA-Seq, ribosome profiling, and microarray analysis. From these studies, we identified changes in mRNA levels and translation of selenoprotein genes and genes regulated by interferon-gamma. Cytokine profiles of serum indicated that interferon-gamma and IL-6 levels were increased in the Se-adequate mice relative to Se-deficient mice.

overall_design: Gene expression analysis of liver and lung tissue from mice fed Se-deficient or Se-adequate diets

first: Petra

last: Tsuji

first: Bradley

last: Carlson

first: Christine

middle: B

last: Anderson

first: Harold

last: Seifried

first: Dolph

last: Hatfield


title: Expression analyses of E12.5 embryonic brains from Nestin Cre+, Rest GTi/GTi vs Rest GTi/GTi litermates

status: Public on Aug 01 2015

city: Portland

first: Tamilla

last: Nechiporuk

state: OR

address: 3181 Sam Jackson Park Road

department: Vollum

institute: OHSU

summary: We use mice containing a gene trap in the first intron of the Rest gene, which effectively eliminates transcription from all coding exons, to prematurely remove REST from neural progenitors.  We find catastrophic DNA damage that occurs during S-phase of the cell cycle and concominant with activation of p53 pro-apoptotic sgnalling, with consequences including abnormal chromosome separation, apoptosis, and smaller brains.

overall_design: extract RNA from E12.5 brain in quadriplicates, compare gene expression profile between Gene Trap REST knockout mice and control littermates

first: Nechiporuk

last: Tamilla

first: McGann

last: James

first: Mullendorff

last: Karin

first: Ronghun

last: Shen

first: Floss

last: Thomas

first: Wurst

last: Wolfgang

first: Mandel

last: Gail


title: The human glioblastoma cell culture resource

first: Sven

last: Nelander

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


title: Transcriptome profiling of deciduas from pre-eclamptic and normotensive pregnancies

status: Public on Aug 05 2015

city: Perth

first: Eric

last: Moses

state: Western Australia

address: Level 5, Medical Research Foundation (MRF) Building, 50 Murray Street

department: Centre for Genetic Origins of Health and Disease

country: Australia

institute: The University of Western Australia

summary:
Genome-wide analysis of decidual transcriptome in pre-eclampsia compared with normotensive controls to find differentially expressed genes/pathways.
Preeclampsia (PE) is a common and serious pregnancy hypertensive disorder with a strong genetic component. The study aims were to use genome-wide analysis of decidual transcriptome in pre-eclampsia compared with normotensive controls to identify differentially expressed biological pathways, and to determine common pathways between the transcriptome and previously identified maternal susceptibility genes.

overall_design: Total RNA from decidua basalis obtained from pre-eclamptic and normotensive control patients at Caesarean section

first: Hannah

last: Yong

first: P

last: Melton

first: M

last: Johnson

first: K

last: Freed

first: B

last: Kalionis

last: Murthi

first: S

last: Brennecke

first: R

last: Keogh


title: Expression data of mESCs differentiated into Paraxial mesoderm

city: ILLKIRCH

first: philippe

last: moncuquet

address: 1 rue laurent fries

country: France

institute: IGBMC

summary: Stem cell-derived tissues have wide potential for modelling developmental and pathological processes as well as cell-based therapy. However, it has proven difficult to generate several key cell types in vitro, including skeletal muscle. In vertebrates, skeletal muscles derive during embryogenesis from the presomitic mesoderm (PSM). Using PSM development as a guide, we establish conditions for the differentiation of monolayer cultures of mouse embryonic stem (ES) cells into PSM-like cells without the introduction of transgenes or cell sorting. We differentiated mouse ESCs in serum-free medium supplemented with Rspo3 ( or as an alternative with Chir 9902) and the Bmp inhibitor LDN193189. In vivo, the PSM cells are first expressing Msgn1 (posterior PSM marker) and then mature to express Pax3 (anterior PSM marker). After 4 days of differentiation of mESCs, Msgn1-positive cells were FACS-sorted and their transcriptome analyzed. After 6 days of differentiation, Pax3-positive cells were sorted and their transcriptome analyzed.

overall_design: Mouse ESCs differentiated for 0, 4 and 6 days in serum-free medium containing a Wnt activator, a BMP inhibitor and DMSO, to study paraxial mesoderm in vitro

first: Jerome

last: Chal

first: Benedicte

last: Gobert


title: High Dose Tamoxifen in the Mouse Gastric Epithelium

status: Public on Jul 31 2015

city: St. Louis

first: Jason

last: Mills

state: Mo

address: Department of Medicine - GI

institute: Washington University in St. Louis

summary: Tamoxifen, a selective estrogen receptor modulator, is widely used in research and clinically in patients. Tamoxifen injection (3 consecutive days, intraperitoneal, 5mg/20g mouse body weight) causes dramatic rearrangement of the gastric mucosa with loss of > 90% of PCs, a 6-fold increase in proliferation in stem/progenitor cells, and morphological changes in the ZCs in the bases of gastric-units.

overall_design: Time course of injection of high-dose tamoxifen. 3 mice were pooled for each condition.

first: Won

last: Huh

first: Benjamin

last: Moore


title: Influence of low and high force muscle activity on paralyzed muscle gene expression

first: Richard

last: Shields

summary: We used a novel approach to study the acute effect of two frequencies of stimulation (20 Hz and 5 Hz; high and low force, respectively) on gene regulation in people with chronic paralysis. Three hours after the completion of the electrical stimulation protocol (5 Hz or 20 Hz), we sampled the vastus lateralis muscle and examined genes involved with metabolic transcription, glycolysis, oxidative phosphorylation, and mitochondria remodelling.  We discovered that the 5 Hz stimulation, despite generating a lower overall force, induced a 5-6 fold increase (p<0.05) in key metabolic transcription factors including PGC-1α, NR4A3, and ABRA.  Neither protocol showed a robust regulation of genes for glycolysis, oxidative phosphorylation, and mitochondria remodelling.

first: Michael

last: Petrie

first: Manish

last: Suneja


title: Expression data of regenerating embryonic mouse hearts

status: Public on Aug 14 2015

city: Gießen

first: Jörg-Detlef

last: Drenckhahn

address: Feulgenstrasse 10-12

department: Department of Pediatric Cardiology

institute: Justus-Liebig-University Gießen

summary: We have recently shown a remarkable regenerative capacity of the prenatal heart using a genetic model of mosaic mitochondrial dysfunction in mice. This model is based on inactivation of the X-linked gene encoding holocytochrome c synthase (Hccs) specifically in the developing heart. Loss of HCCS activity results in respiratory chain dysfunction, disturbed cardiomyocyte differentiation and reduced cell cycle activity. The Hccs gene is subjected to X chromosome inactivation, such that in females heterozygous for the heart conditional Hccs knockout approximately 50% of cardiac cells keep the defective X chromosome active and develop mitochondrial dysfunction while the other 50% remain healthy. During heart development, however, the contribution of HCCS deficient cells to the cardiac tissue decreases from 50% at midgestation to 10% at birth. This regeneration of the prenatal heart is mediated by increased proliferation of the healthy cardiac cell population, which compensate for the defective cells and allow the formation of a fully functional heart at birth. Here we performed microarray expression ananlyses on 13.5 dpc control and heterozygous Hccs knockout hearts to identify molecular mechanisms that drive embryonic heart regeneration.

overall_design: 13.5 dpc hearts of heterozygous heart conditional Hccs knockout and littermate control female embryos were dissected, RNA was isolated and hybridized to Affymetrix arrays. At this developmental stage the most dramatic changes in tissue composition occur in the knockouts, as hyperproliferation of healthy cardiomyocytes is readily detectable while a substantial contribution of HCCS deficient cells is still present. 5 biological replicates per genotyp each containing 4-5 pooled hearts were analyzed.

first: Manuela

last: Magarin


title: Microarray analysis of the skin of P2.5 K5cre-caNrf2 mice

city: Zurich

first: Matthias

last: Schäfer

address: Otto-Stern-Weg 7

country: Switzerland

institute: ETH Zurich

summary: The Nrf2 transcription factor is a key player in the cellular stress response, which regulates the expression of important antioxidant enzymes and other cytoprotective proteins. We recently generated a novel transgenic mouse model to determine the function of Nrf2 in the skin. These mice show reduced number of apoptotic keratinocytes after UVB irradiation due to enhanced ROS detoxification. They also show enhanced tumorigenesis in the HPV8 tumor model.

overall_design: RNA from whole skin of 3 single P2.5 K5cre-caNrf2 (tg/tg) and 3 single P2.5 K5cre-wt (tg/wt=control) mice were used

first: F

last: Rolfs

last: Werner

last: Zoller

first: C

last: Aquino

first: H

last: Rehrauer


title: Gene expression changes induced by expression of dMPL in murine bone haematopoietic progenitor cells

city: Hannover

first: Adrian

last: Schwarzer

address: Carl-Neuberg-Str. 1

department: Experimental Hematology

institute: Hannover Medical School

summary: Thrombopoietin (Thpo) signals via its receptor Mpl and regulates megakaryopoiesis, hematopoietic stem cell (HSC) maintenance and post-transplant expansion. Mpl expression is tightly controlled and deregulation of Thpo/Mpl-signaling is linked to hematological disorders. Here, we constructed an intracellular-truncated, signaling deficient Mpl protein which is presented on the cell surface (dnMpl). The transplantation of bone marrow cells retrovirally transduced to express dnMpl into wildtype mice induced thrombocytopenia, and a progressive loss of HSC. Functional analysis of the truncated Mpl in vitro and in vivo demonstrated no internalization after Thpo binding and the inhibition of Thpo/Mpl-signaling in wildtype cells due to dominant-negative (dn) effects by receptor competition with wildtype Mpl for Thpo binding. Gene expression analysis was performerd of Lin-Sca1+cKit+ (LSK) cells isolated from mice transplanted with dnMpl transduced BM cells. The gene expression profile supported the exhaustion of HSC due to increased cell cycle progression and identified new and known downstream effectors of Thpo/Mpl-signaling in HSC (namely TIE2, ESAM1 and EPCR detected on the HSC-enriched LSK cell population). In summary, we established a novel way of Thpo/Mpl inhibition in the adult mouse and performed in depth analysis of the phenotype including gene expression profiling.

overall_design: BM cells were flushed from the femurs and tibias of C57Bl/6 donor mice. Lineage-marker negative (lin-) cells were isolated by magnetic cell sorting using lineage-specific antibodies (GR1, CD11b, CD45R/B220, CD3e, TER-119). Prior to viral transduction, lin- BM cells were prestimulated for 24-48h in StemSpan, containing 10 ng/ml murine SCF, 20 ng/ml murine Thpo, 10 ng/ml recombinant human FGF-1, 20 ng/ml murine IGF2, 1% penicillin/streptomycin, 2 mM glutamine. Lin- cells were transduced twice on two following days with an MOI of 10 with retroviral vectors on Retronectin coated and preloaded wells (10 μg/cm2). On day four after isolation, 5x10^5 cells/mouse were intravenously injected into lethally irradiated C57Bl/6 mice (10 Gy). Eight weeks after transplantation Lin-Sca1+cKit+ (LSK) cells were isolated from dnMpl and control transplanted mice by fluorescent activated cell sorting. For each sample, BM of 2-5 mice were pooled. RNA was isolated using RNeasy Micro Kit (Qiagen GmbH, Hilden, Germany). RNA quality was assessed using the Agilent 2100 Bioanalyzer.

first: Ute

last: Modlich


title: Mir-30e* is an independent subtype-specific prognostic marker in breast cancer

city: Milan

first: Francesca

last: D'Aiuto

address: Via Amadeo, 42

department: Department of Experimental Oncology and Molecular Medicine

country: Italy

institute: Fondazione IRCCS Istituto Nazionale dei Tumori

summary: Both gene and miRNA expression patterns separately correlate with survival in breast cancer suggesting that the development of models using both miRNAs and gene markers might improve their prediction performance. In this study miRNAs significantly associated with development of distant metastasis were identified and further investigated and validated in the publicly available dataset from the METABRIC. A combined outcome prediction model using gene expression, miRNA expression and clinico-pathological features was implemented.

overall_design: Fresh-frozen primary tumors were obtained from 123 patients with operable breast cancer previously untreated, pathologically defined as axillary node-negative and undergoing radical or conservative surgery at the Istituto Nazionale Tumori of Milano (INTM) between1990 and 1998. Patients were selected in order to have a comparable pattern of classical risk factors (age, tumor size).

first: Maurizio

last: Callari

first: Vera

last: Cappelletti

first: Maria

last: Daidone


title: Gene expression profile of the neonatal female mouse brain after administration of testosterone propionate.

city: Kumamoto

first: Yutaka

last: Nakachi

address: 1-1-1 Honjo, Chuo-ku

department: Faculty of Life Sciences

institute: Kumamoto University

summary:
The aim of this study is to investigate the gene expression profiles during masculinization of neonatal female mice brain by exogenous androgen treatment.
The results of our expression analysis will shed light on the identification of the key molecules of sexual differentiation of mammalian brain.

overall_design: Expression microarray analysis was performed using the RNAs extracted from the brains of neonatal mice treated with intraperitoneal injection of testosterone propionate during sex determination period of mice brain.

first: Mioko

last: Iseki

first: Tomotaka

last: Yokoo

first: Yosuke

last: Mizuno

first: Yasushi

last: Okazaki


title: Expression data from DCs stimulated with  LPS vs DCs stimulated with PTX

city: shanghai

first: haiyan

last: zhou

address: No.320Yueyang Road

institute: Shanghai Institute of Biochemistry and Cell Biology

summary: DCs treated with PTX (PTX-DC) is able to induce EAE like PTX as adjuvant whereas neither LPS nor DCs treated with LPS (LPS-DC) fails to induce EAE. We want to identify genes that are responsible for EAE induction in DCs and genes that are able to toloerize EAE in DCs through the microarray.

overall_design: Bone marrow derived dendritic cells are either unstimulated or stimulated with LPS and PTX for 24h respectively. Cells are harveseted for RNA extraction and hybridization on Affymetrix microarrays.

first: Haiyan

last: Zhou

first: Yanming

last: Wang


title: Hhex and Cer1 Mediate the Sox17 Pathway for Cardiac Mesoderm Formation in Embryonic Stem Cells

status: Public on Jul 30 2015

city: London

first: Michael

middle: D.

last: Schneider

address: Du Cane Road

department: Imperial Centre for Translational and Experimental Medicine

institute: Imperial College London

summary:
Cardiac muscle differentiation in vivo is guided by sequential growth factor signals, including endoderm-derived diffusible factors, impinging on cardiogenic genes in the developing mesoderm. Previously, by RNA interference in AB2.2 mouse embryonic stem cells (mESCs), we identified the endodermal transcription factor Sox17 as essential for Mesp1 induction in primitive mesoderm and subsequent cardiac muscle differentiation. However, downstream effectors of Sox17 remained to be proven functionally. In this study, we used genome-wide profiling of Sox17-dependent genes in AB2.2 cells, RNA interference, chromatin immunoprecipitation, and luciferase reporter genes to dissect this pathway. Sox17 was required not only for Hhex (a second endodermal transcription factor) but also for Cer1, a growth factor inhibitor from endoderm that, like Hhex, controls mesoderm patterning in Xenopus toward a cardiac fate. Suppressing Hhex or Cer1 blocked cardiac myogenesis, although at a later stage than induction of Mesp1/2. Hhex was required but not sufficient for Cer1 expression. Over-expression of Sox17 induced endogenous Cer1 and sequence-specific transcription of a Cer1 reporter gene. Forced expression of Cer1 was sufficient to rescue cardiac differentiation in Hhex-deficient cells. Thus, Hhex and Cer1 are indispensable components of the Sox17 pathway for cardiopoiesis in mESCs, acting at a stage downstream from Mesp1/2.
Keywords: Cardiac development, Embryonic stem cells, Endoderm, Myogenesis, RNA interference

overall_design:
Genome-wide expression profiling of Sox17-dependent genes.
Mouse embryonic stem cells expressing Sox17 or luciferase shRNA were differentiated for up to 10 days by the embryoid body method [PMID:8155574], then were analysed using Affymetrix microarrays.
ESCs were transduced with lentiviral vectors coexpressing enhanced green fluorescent protein (eGFP) with shRNA against Sox17, or against firefly luciferase. Transduced cells were flow-sorted based on GFP fluorescence, grown as embryoid bodies, and transferred to tissue culture plates after 4.5 days [PMID:17360443]. Cells were harvested at days 0, 2, 4, 5, 6, 8 and 10 in two biological replicates, except where noted.

first: Yu

last: Liu

first: Ruri

last: Kaneda

first: Thomas

last: Leja

first: Tatiana

last: Subkhankulova

first: Oleg

last: Tolmachov

first: Gabriella

last: Minchiotti

first: Robert

last: Schwartz

first: Mauricio

last: Barahona


title: Expression profile of COUP-TFII overexpressing hearts

status: Public on Jul 24 2015

city: Houston

first: San-pin

last: Wu

state: TX

address: 1 Baylor Plaza

institute: Baylor College of Medicine

summary: Increased COUP-TFII levels are found in human dilated cardiomyopathy as well as in mouse models that develop cardiomyopathy. COUP-TFII overexpression in adult mouse hearts caused ventricular dilation and compromised cardiac functions. To gain insights on COUP-TFII’s effect in hearts, we identified the molecular profile of COUP-TFII overexpressing hearts through microarray analysis. The result may shred light on molecular mechanisms that mediate development of dilated cardiomyopathy.

overall_design: We utilized a previously established CAG-S-COUP-TFII allele and crossed it with the Myh6-MerCreMer (Myh6-MCM) line to overexpress COUP-TFII specifically in cardiomyocytes at two months of age by administration of tamoxifen. The experimental group has genotype of Myh6-MCM; CAG-S-COUP-TFII while the control group consists of Myh6-MCM mice (Figure 1C). Whole ventricles were harvested 16 days post induction for molecular profiling.

first: Sophia

middle: Y

last: Tsai

first: Ming-jer


title: Distinct signal transduction pathways downstream of the (P)RR revealed by microarray and ChIP-chip analyses [Expt: siRNA]

city: Berlin

first: Daniela

last: Zaade

address: Hessische Straße 3-4

department: Center for Cardiovascular Research

institute: Charité

summary: Within the overall project, we performed a set of microarray and chromatin-immunoprecipitation (ChIP)-chip experiments using siRNA against the (pro)renin receptor ((P)RR), stable overexpression of PLZF, the PLZF translocation inhibitor genistein and the specific V-ATPase inhibitor bafilomycin to dissect transcriptional pathways downstream of the (P)RR.

overall_design:
In this dataset, we include the expression data obtained from siRNA against (P)RR in KELLY cells.Three intervention samples and three control samples were analyzed. We generated the following pairwise comparisons using Chipinspector (Genomatix Software GmbH) and a FDR of 2%.
ChipInspector carries out significance analysis on the single probe level. Normalized probe set level data not provided for individual Sample records. Processed data is available on Series record.

first: Heiko

last: Funke-Kaiser


title: Distinct signal transduction pathways downstream of the (P)RR revealed by microarray and ChIP-chip analyses [Expt: PLZF_KELLY]

overall_design:
In this dataset, we include the expression data obtained from stable PLZF overexpression in KELLY cells and from respective insertless controls. Two intervention samples and two control samples were analyzed. We generated the following pairwise comparisons using Chipinspector (Genomatix Software GmbH): FK_2, FK_10 versus FK_3, FK_11.
ChipInspector carries out significance analysis on the single probe level. Normalized probe set level data not provided for individual Sample records. Processed data is available on Series record.


title: Hepatic gene expression in C56BL/6J mice fed a quercetin diet for 20 weeks

city: Tsukuba

first: Masuko

last: Kobori

state: Ibaraki

address: 2-1-13 Kannondai

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

summary:
Both the 0.05% and 1% querceitn diets did not significantly affect the body weight, fat accumulation, and blood components. However, 0.05% quercetin significantly increased the glutathione/oxidized glutathione ratio in the liver. Moreover, the 1% quercetin diet reduced the lipid peroxidation markers 8-isoprostane in plasma and malondialdehyde in the liver, epididymal adipose tissues, and small intestine.
Although comprehensive gene expression analysis dot not detect the genes with significantly different expression levels among the groups of mice, RT-PCR analysis showed that the 1% quercetin diet significantly induced the expression of the antioxidant enzymes Gpx1, Cat, and Sod1 in the liver and Gpx1 and Cat in the epididymal adipose tissues. The transcription factor nuclear factor E2-related factor 2 (Nrf2) was slightly induced in the nuclear fraction of the livers of mice fed the 1% quercetin diet. Quercetin may induce antioxidant enzymes by directly or indirectly activating the Nrf2 pathway in the liver.

overall_design: Five-week-old male mice were fed a AIN-93G diet containing 0% (Control), 0.05% (0.05% quercetin diet), or 1% quercertin  (1% quercetin diet) for 20 weeks.


title: Effects of Arid1a knockout in murine ovarian endometrioid carcinomas with biallelic inactivation of Apc and Pten

status: Public on Aug 04 2015

city: Ann Arbor

first: Rork

last: Kuick

state: MI

address: University of Michigan, SPH II, 1415 Washington Heights, Room M2533

institute: University of Michigan

summary: We mated mice with floxed alleles of both Apc and Pten, to mice with floxed alleles for Arid1a, to obtain female mice with both copies of all three genes floxed.  At 7 to 8 weeks of age the right ovarian bursal cavites of the mice were injected with 50 million plaque-forming units of adenovirus expressing Cre recombinase, which causes the floxed genes to be knocked out.  Tumor tissue from 3 mice for each group was obtained at necropsy, RNA purified, and targets for Affymetrix arrays synthesized from the mRNAs.  We used Affymetrix Mouse Genome 430 2.0 arrays, which hold 45101 probe-sets.  Raw data was processed with Robust Multi-array Average algorithm (RMA).  Data is log2-transformed transcript abundance estimates. We performed T-tests to compare the 3 vs 3 arrays.  We supply a supplementary excel workbook that holds the same data as the data matrix file, but also holds the probe-set annotation at the time we analyzed the data, and some very simple statistical calculations, which select subsets of the probe-sets as differentially expressed.  Consumers should consider obtaining more up-to-date probe-set annotation for the array platform. We have also supplied a second supplementary tar archive holding software and files to 1) perform permutation testing of the probe-set selection in order to estimate false discovery rates for the probe-sets we selected as differentially expressed, 2) perform enrichment testing of GO terms, and 3) to perform enrichment testing of KEGG pathways and 3000 curated gene sets from version 4 of the Molecular Signatures Database (MSigDB). The software is in "C".

overall_design: Ovarian endometrioid carcinoma samples from 3 female mice with conditional knockout of Apc and Pten, were compared to similar tumors from 3 female mice with conditional knockout of Apc, Pten, and Arid1a.

first: Yali

last: Zhai

first: Isao

last: Sakaguchi

first: Courtney

last: Tipton

first: Rong

first: Zhong

first: Suzanne

last: Baker

first: Eric

last: Fearon

first: Kathleen

last: Cho


title: Leishmania major modulates autophagy in host macrophages during intracellular differentiation

city: Würzburg

first: Claus

middle: Juergen

last: Scholz

address: Josef-Schneider-Str. 2

department: Core Unit SysMed

institute: University Hospital Würzburg

summary:
Autophagy generally participates in innate immunity by elimination of intracellular pathogens. However, many of them developed successful strategies to counteract their autolysosomal digestion and lastly to exploit this catabolic cellular process.
Protozoan parasites of the genus Leishmania are the causative agent of leishmaniasis, one of the 13 most important tropical diseases. Leishmania persists as endo-parasite in host macrophages, where it uses multiple strategies to manipulate the microbicidal host cell functions and to escape from the host immune system. Understanding how Leishmania interacts with host macrophages during uptake, differentiation, intracellular replication, and release might be the key to develop new drugs in target-directed approaches to treat patient with leishmaniasis.

overall_design: Here, we generated expression profiles from bone marrow-derived macrophages (BMDM) at 1h and 24h post infection (p.i.) with Leishmania major and respective controls.

first: Benjamin

last: Frank

first: Heike

last: Weber

first: Uta

last: Schurigt


title: Effect of NDRG3 or HIF-1α knockdown on cell response to hypoxia

city: Daejeon

first: Minho

last: Kang

address: 125 Gwahak-ro, Yuseong-gu

department: Medical Genomics Research Center

country: South Korea

institute: KRIBB

summary: Analysis of Huh-7 hepatocarcinoma cell line depleted of NDRG3 or HIF-1α under hypoxic condition. HIF-1α and NDRG3 have distinct functions in hypoxia responses. Results provide insight into molecular basis of HIF-independent signaling in the development and progression of hypoxic tumors

overall_design: Gene expression profiles of Huh-7 cells stably expressing NDRG3-shRNA or HIF-1α-shRNA under normoxia were compared to gene expression profiles of Huh-7 stable cells under  hypoxia for 6, 12 and 24 hours.

first: Dong

last: Lee

first: Ye

middle: J

last: Jang

first: Young

middle: I

last: Yeom


title: Gene expression in E10.5 Maxillary Arch Mesenchyme from control and Lhx6-/-;Lhx8-/- mutant embryos

status: Public on Jul 23 2015

city: New York

first: Juhee

last: Jeong

state: New York

address: 345 E 24th St

department: Basic sciences and Craniofacial development

institute: New York University College of Dentistry

summary:
We used laser capture microdissection to isolate maxillary arch mesenchyme from E10.5 embryos.  This tissue was collected from both control (3x) and Lhx6-/-;Lhx8-/- mutant (3x) samples.
Transcriptional profiling was performed using Affymetrix GeneChip Mouse Genome 430 2.0 arrays.

overall_design:
The mutant mice are of mixed genetic background of C57BL/6J, 129 and CD-1 strains.  The head of E10.5 embryos was collected and embedded in Optimal Cutting Temperature resin (Tissue-Tek) by flash freezing on dry ice. The frozen sections were collected on polyethylene naphthalate membrane slides (Leica). Leica LMD6000 Laser Micro-Dissection System was used to cut out the normal expression domain of Lhx6 and Lhx8 in the maxillary arch mesenchyme. The tissue was collected from the entire antero-posterior extent of the maxillary arches. Total RNA was extracted using RNeasy Micro Kit (Qiagen). Subsequent steps of transcriptional profiling were performed by the New York University Genome Technology Center, beginning with the amplification of RNA by Ovation Nano Amplification system (NuGen). RNA samples from three wild-type and three Lhx6−/−;Lhx8−/− mutant embryos, all somite count- and sex-matched (females), were analyzed with Affymetrix GeneChip Mouse Genome 430 2.0 arrays.
A list of Lhx-regulated genes were generated from the microarray result based on the following criteria: fold change in the average expression between wild types and Lhx6−/−;Lhx8−/− mutants is >1.5, the difference is statistically significant (P < 0.05) and the average intensity of the probe signal is >100 for wild-type and/or mutant samples. The resulting list of 212 genes was used for a gene ontology analysis with DAVID (27,28).

first: Jeffry

last: Cesario


title: Effect of NDRG3 over-expression and knockdown on cell response to hypoxia

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

overall_design: Refer to individual Series


title: Gene and microRNA expression data from tumor induced CD11b+ MDSC

city: Padova

first: Stefania

last: Bortoluzzi

address: via G. Colombo 3

department: Department of Molecular Medicine

institute: University of Padova

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

summary:
Tumor growth is associated with a profound alteration of myelopoiesis, leading to recruitment of immunosuppressive cells known as myeloid-derived suppressor cells (MDSCs). Immuno-regulatory activity of both tumor-induced and BM-derived MDSCs (by GM-CSF and IL-6 treatment) was entirely dependent on C/EBP transcription factor (TF), a key component of the emergency myelopoiesis triggered by stress and inflammation. We used miR expression analysis to identify miRs which could drive MDSC recruitment/generation/activity by modulating specific TFs and pathway. In particular, we identified a miR signature of 79 miR differentially expressed between not suppressive CD11b+ cells and CD11b+ isolated from tumor mass and spleen of tumor-bearing mice. Moreover on the same samples we profiled gene expression with Affymetrix microarrays to perform an integrated analysis of mirna and gene expression.

Keywords: Expression profiling by array

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

overall_design: CD11b+ cells were immuno-magnetically enriched from various mouse tissues, and total RNA isolated by Trizol reagent. CD11b+ cells obtained from the spleen of healthy BALB/c and C57BL/6 mice were used as reference sample for tumor induced CD11b+ MDSC, enriched from either the spleen and the tumor infiltrate of tumor-bearing mice. A triplicate of each sample was considered (except for EL4 samples, where we considered a duplicated), and each sample derives from a pool of three mice, at least.

first: Francesco

last: Marincola

first: Francesca

last: Simonato

first: Elisa

last: Peranzoni

first: Bianca

last: Calì

first: Ena

last: Wang

first: Luigi

last: Naldini

first: Bernhard

last: Gentner

first: Christian

last: Trautwein

first: Ilaria

last: Marigo

last: Dolcetti

first: Stefano

last: Ugel

first: Nada

last: Sonda

first: Silvio

last: Bicciato

first: Paola

last: Zanovello

first: Susanna

last: Mandruzzato

first: Andrea

last: Bisognin

first: Vincenzo

last: Bronte


title: Expression data from Williams-Beuren Syndrome ES cell line (ESSP9)

status: Public on Jul 16 2015

city: Barcelona

first: Victoria

last: Campuzano

address: Dr Aiguader, 88

department: CEXS

country: Spain

institute: Universitat Pompeu Fabra

summary: Data present the expression analysis of two biological replicates of a mouse ES cell line with hemizygous deletion of WBSCR

overall_design: We used microarrays to detail the global programme of gene expression underlying WBS phenotype and identified distinct classes of deregulated genes.

first: Maria

last: Segura


title: FGF2 cooperates with IL-17A to promote intestinal epithelium wound healing

city: Shanghai

first: Xinyang

last: Song

address: 320 Yue Yang Road

department: Institute of Health Sciences

institute: Shanghai Institutes for Biological Sciences

summary: The intestinal epithelial barrier plays a critical role in the mucosal immunity. However, it remains largely unknown how the epithelial barrier is maintained after damage. Here we show that FGF2 synergizes with IL-17A to induce genes for repairing of damaged epithelium. Deficiency of FGF2 or IL-17A resulted in impaired epithelial proliferation, increased pro-inflammatory microbiota outgrowth, and consequently worse pathology in a DSS-induced colitis model.

overall_design: Mouse primary intestinal epithelial cells left untreated (UN) or stimulated for 6 hr with IL-17A (50 ng/ml), FGF2 (5 ng/ml), or both (IL-17A plus FGF2).

first: Youcun

last: Qian


title: Expression data from quadriceps of utrn+/-;mdx mice treated with spironolactone plus lisinopril compared to untreated

status: Public on Jul 17 2015

city: Columbus

first: Jill

last: Rafael-Fortney

state: OH

address: 460 W. 12th Ave

department: Physiology & Cell Biology

institute: The Ohio State University

summary: To identify the gene expression differences in skeletal muscles resulting from treatment of dystrophic mice with spironolactone plus lisinopril

overall_design: 6 total samples were analyzed; 3 biological replicates for each spironolactone plus lisinopril and untreated groups; a pairwise comparison between groups was carried out and a fold-change ≥2 were selected.

first: Jessica

last: Chadwick

first: Denis

last: Guttridge


title: Differential gene expression of meiotic drive system of Aedes aegypti

status: Public on Jul 15 2015

city: Columbia

first: Susanta

middle: K.

last: Behura

state: Missouri

address: 920 East Campus Drive

department: Division of Animal Sciences

institute: Univeristy of Missouri

summary: We conducted a whole transcriptome analysis of testes from a meiotic drive-carrying strain (T37) in comparison with a drive-sensitive strain (RED) using microarrays based on the complete annotated Ae. aegypti gene set. The T37 strain, which carries a strong meiotic drive gene (Mori et al., 2004 (PMID 15605641)), was established from mosquitoes collected in Trinidad. The RED strain is highly sensitive to the meiotic drive gene (Hickey and Craig, 1966 (PMID ); Mori et al., 2004 (PMID 15605641)).

overall_design: A six-chip study using total RNA recovered from three biological samples of the T37 strain and another three biological samples of the Red strain of Aedes aegypti. Each chip measures the expression level of 16,092 genes annotated from the Aedes aegypti genome sequence, with twenty 60-mer probe pairs (PM/MM) per gene, with three-fold technical redundancy.

first: Dongyoung

last: Shin

first: Akio

last: Mori

first: David

last: Severson


title: MicroRNA-203 represses selection and expansion of oncogenic HRas transformed tumor initiating cells [array]

city: Aurora

first: Kent

middle: Augustus

last: Riemondy

state: Colorado

department: Biochemistry and Molecular Genetics

institute: University of Colorado School of Medicine

summary: In many mouse models of skin cancer, only a few tumors typically form although many cells competent for tumorigenesis receive the same oncogenic mutations. These observations suggest a selection process for defining tumor initiating cells. Here we use quantitative mRNA- and miR-Seq to determine the impact of HRasG12V on the transcriptome of keratinocytes. We discover that microRNA-203 is downregulated by HRasG12V. Using a knockout mouse model, we demonstrate that loss of microRNA-203 promotes selection and expansion of tumor-initiating cells. Conversely, restoration of microRNA-203 with an inducible model potently inhibits proliferation of these cells. We comprehensively identify microRNA-203 targets required for HRas-initiated tumorigenesis. These targets include important effectors of the Ras pathway and essential genes required for cell division. Together, this study establishes a role for the loss of microRNA-203 in promoting selection and expansion of HRas mutated cells and identifies a mechanism through which microRNA-203 antagonizes HRas-mediated tumorigenesis.

overall_design: Identifying mRNA and microRNA networks regulated by oncogenic HRasG12V in primary keratinocytes through the use of 3Seq and small-RNA-Sequencing. Additionally we utilize ribosome-profiling, 3Seq, Microarray and Ago2-HITS-CLIP approaches to identify novel miR-203 target genes.

first: Rui

last: Yi


title: Effect of rapamycin and KU-0063794 on CTL gene expression

city: Dundee

first: Jens

middle: Ludger

last: Hukelmann

state: Angus

address: Dow Street

department: Centre for Gene Regulation and Expression

institute: University of Dundee

summary:
Comparison of transcriptional profile of CD8 cytotoxic T lymphocytes terated with the mTORC1 inhibitor rapamycin or the mTOR inhibitor KU-0063794 and comparison with proteomic analysis.
Abstract: High resolution mass spectrometry maps the cytotoxic T lymphocyte (CTL) proteome and the impact of mammalian target of rapamycin complex 1 (mTORC1) on CTL. We show that the CTL proteome is dominated by metabolic regulators and granzymes and that mTORC1 selectively represses and promotes expression of a protein subset (~10%) including key CTL effector molecules and signaling proteins. mTORC1 also controlled flux through a subset of metabolic pathways rather than acting as an on/off switch for global CTL metabolism. Proteomic data highlighted the potential for mTORC1 negative control of phosphatidylinositol (3,4,5)-trisphosphate (PIP3) production in CTL. Further work revealed that mTORC1 represses PIP3 production and determines the mTORC2 requirement for activation of the serine/threonine kinase AKT. Unbiased proteomic analysis thus provides a comprehensive understanding of CTL identity and mTORC1 control of CTL function.

overall_design: Spleens from three biological replicates (control and drug treated samples were generated from the same spleens) from P14 TCR transgenic mice were harvested and activated with the antigenic peptide gp33-41 and IL-2/12 for 48h. After activation, cells were further clonally expanded in the presence of IL-2/12 for a further 96h prior to RNA extraction and hybridization to Affymetrix microarray.

middle: L

first: Doreen

middle: A

last: Cantrell


title: Expression data from haploid and diploid epiblast stem cells

city: Beijing

first: Ling

last: Shuai

address: 1 Beichen West Road, Chaoyang District, Beijing 100101, P.R.China

institute: Chinese Academy of Sciences

summary: Haploid pluripotent stem cells, such as haploid embryonic stem cells (haESCs), facilitate the genetic study of recessive traits. In vitro, fish haESCs maintain haploidy in both undifferentiated and differentiated states, but whether mammalian haESCs can preserve pluripotency in the haploid state has not been tested. Here, we report that mouse haESCs can differentiate in vitro into haploid epiblast stem cells (haEpiSCs), which maintain an intact haploid genome, unlimited self-renewal potential, and durable pluripotency to differentiate into various tissues in vitro and in vivo. Mechanistically, the maintenance of self-renewal potential depends on the Activin/bFGF pathway. We further show that haEpiSCs can differentiate in vitro into haploid progenitor-like cells.

overall_design: haploid and diploid epiblast stem cells

first: Qi

last: Zhou


title: Mitochondrial gene expression decline in aging is tissue-specific and independent of mitochondrial number

status: Public on Jul 03 2015

city: Seattle

first: James

middle: William

last: MacDonald

state: WA

address: 4225 Roosevelt Way NE

department: Environmental and Occupational Health Sciences

institute: University of Washington

summary:
Aging is the progressive decline in organismal function that leads to an increased risk of multiple diseases and mortality. The molecular basis of this decline is unknown. Using quantitative PCR for mitochondrial mRNA from multiple tissues from the same animals, we found that the rate of change in mouse mitochondrial expression is tissue-specific, with cardiac expression declining early (8-10 months), adipose expression declining late (25-30 months), and no change in kidney or skin. In cardiac tissue, mitochondria-derived mRNA levels declined more slowly than nuclear encoded mRNAs, suggesting a potential dysregulation. These changes were independent of alteration in mitochondrial number, as measured by quantitative PCR of mitochondrial DNA and citrate synthase activity. We found no change in the variability between mitochondrial mRNA levels with age, suggesting that the changes are not due to random dysregulation at the level of gene expression. Caloric restriction (CR), a lifespan-extending intervention proposed to act through mitochondrial biogenesis, delayed the decline in both cardiac and adipose mitochondrial mRNA levels of F344 rats. CR caused an increase in citrate synthase activity but did not alter mitochondrial DNA content, indicating increased translation or reduced turnover of mitochondrial proteins. These results demonstrate that mitochondrial gene expression changes with age are not coupled to mitochondrial number, are likely to be regulated, and are governed by tissue-specific processes. These findings indicate that aging is neither a programmed organism-wide change orchestrated in a top-down fashion nor a product of random dysregulation of gene expression but that tissue-specific factors may independently control aging in different organ compartments.

Keywords: aging

overall_design: Cardiac ventricle total RNA from 10 young (4-6 month) and 10 young (25-28 month) mice were compared.

first: Richard

middle: P

last: Beyer


title: Tbx15 Controls Skeletal Muscle Fiber Type Determination and Muscle Metabolism

city: Boston

first: Kevin

middle: Yu-sun

last: Lee

state: MA

address: 1 Joslin Place

institute: Joslin Diabetes Center

summary: Skeletal muscle is composed of both slow-twich oxidative myofibers and fast-twitch glycolytic myofibers that differentially impact muscle metabolism, function, and eventually whole-body physiology. In the present study, we find that the mesodermal transcription factor T-box 15 (Tbx15) is highly and specifically expressed in glycolytic myofibers. Ablation of Tbx15 in vivo leads to a decrease in muscle size due to a decrease in the number of glycolytic fibers, associated with a small increase in the number of oxidative fibers. This shift in fiber composition results in muscles with slower myofiber contraction and relaxation, and also results in decreased whole-body oxygen consumption, decreased spontaneous activity, increased adiposity, and glucose intolerance. In order to identify genes regulated by Tbx15, we utilized C2C12 myoblasts with either a stable retroviral over-expression or stable lentiviral knockdown of Tbx15.

overall_design: RNA was extracted and biotin labelled complementary RNA (cRNA) was prepared from three independent transfections of the four stable C2C12 myoblast cell lines: shTbx15, shGFP, pBABE-Empty-puro, pBABE-Tbx15-puro. Cells were collected at 90% confluency, and subjected to microarray analysis.  Affymetrix M430 2.0 Chips were used.

first: Manvendra

middle: K

last: Singh

first: Siegfried

last: Ussar

first: Petra

last: Wetzel

first: Michael

last: Hirshman

first: Laurie

last: Goodyear

first: Andreas

last: Kispert

first: C

middle: R

last: Kahn


title: Expression data for Fat storage inducing transmembrane protein 2 (FIT2/FITM2)-deleted small intestine

city: Singapore

first: David

last: Silver

address: 8 College Road

country: Singapore

institute: Duke-NUS Graduate Medical School

summary:
Tamoxifen- induced FIT2 deletion using whole body inducible ROSA26CreERT2 FIT2 floxed mice causes upregulation of the p53 pathway which accompanies intestinal death
We used microarrays to detail the changes in small intestine gene expression at day 2, 3, and 5 of tamoxifen induced FIT2 deletion in whole body inducible ROSA26CreERT2 FIT2 floxed mice.

overall_design: Small intestine was harvested from L/L and ROSA26CreERT2 L/L mice at days 2, 3, and 5 post- tamoxifen treatment and subject to microarray analysis. Pooled intestinal RNA from n biological replicates were used for each genotype and timepoint. D2 L/L n=6, D2 KO n=7, D3 L/L n=6, D3 KO n=6, D5 L/L n=8, D5 KO n=7.

first: Vera

last: Goh


title: Gene expression data from LCMV-specific WT and Tcf7-/- follicular T helper cells

city: Chongqing

first: Xinyuan

address: 30 Gaotanyan Street

department: Institute of Immunology, PLA

institute: Third Military Medical University

summary: We did microarray experiments to elucidate the transcriptome changes due to TCF-1 deficiency in Tfh cells. These data clearly demonstrate that Tfh-associated genes were down-regulated in TCF-1-null Tfh cells, whereas Th1-associated signatures were up-regulated, indicating that TCF-1 initiates the Tfh fate by directly strengthening Tfh signatures while suppressing Th1-associated genes.

overall_design: We first sorted WT and TCF-1-null Tfh cells (2 samples per group, each sample was pooled from 4 mice) at day 8 after LCMV Armstrong infection. Then, we extracted RNA, which were subsequently sent to microarray analysis.

first: Lilin

last: Ye

first: Yuzhang

last: Wu


title: ND and HFD memory phenotype CD4 T cells

status: Public on Jul 02 2015

city: Chiba-city

first: Yusuke

last: ENDO

state: Chiba

address: 1-8-1 Inohana, Chuo-ku

department: Immunology

institute: Chiba University

summary: We used microarray analysis to identify specific molecular mechanisms controlling Th17 cell differentiation in HFD mice

overall_design: Memory phenotype CD4 T cells derived from ND or HFD mice were selected for RNA extraction and hybridization on Affymetrix microarrays.

last: Endo

first: Hikari

last: Asou

first: Nao

last: Matsugae

first: Kiyoshi

last: Hirahara

first: Kenta

last: Shinoda

first: Damon

last: Tumes

first: Hirotake

last: Tokuyama

first: Koutaro

last: Yokote

first: Toshinori

last: Nakayama


title: Interferon-Gamma- and Murine-CMV-Activated Primary Macrophages

status: Public on Jul 10 2015

city: Edinburgh

first: Nigel

last: Binns

address: The Chancellor's Building, 49 Little France Crescent

department: Division of Pathway Medicine

institute: The University of Edinburgh