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Mus musculus
6 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Expression profiling of cultured HL-1 cardiomyocytes subjected to hypoxia for 8 hours.
Publication Title
The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 39 Downloadable Samples
NextSeq 500
Description
Gnotobiotic mice have been mono- and bi-colonized with Prevotella copri and Bacteroides thetaiotaomicron to study the affect of those bacteria on mouse glucose homeostasis. Total RNA was extrcated from proximal colon and liver of those mice and germ- free mice.
Publication Title
No associated publication
Sample Metadata Fields
Sex, Age, Specimen part, Cell line
View Samples- Mus musculus, Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
The histone demethylase JMJD2B regulates endothelial-to-mesenchymal transition.
Sample Metadata Fields
Age, Specimen part, Cell line, Treatment
View Samples
GSE107033- Homo sapiens
- 11 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
The lncRNA GATA6-AS epigenetically regulates endothelial gene expression via interaction with LOXL2.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 12 Downloadable Samples
Affymetrix Human Human Exon 1.0 ST Array (huex10st)
Description
Endothelial cells play an important role in maintenance of the vascular system and the repair after injury. Under pro-inflammatory conditions, endothelial cells can acquire a mesenchymal phenotype by a process named endothelial-to-mesenchymal transition (EndMT), which affects the functional properties of endothelial cells. Here, we investigated the epigenetic control of EndMT. We show that the histone demethylase JMJD2B is induced by EndMT promoting pro-inflammatory and hypoxic conditions. Silencing of JMJD2B reduced TGF-β2-induced expression of mesenchymal genes and prevented the alterations in endothelial morphology and impaired endothelial barrier function. Endothelial-specific deletion of JMJD2B in vivo confirmed a reduction of EndMT after myocardial infarction. EndMT did not affect global H3K9me3 levels but induced a site-specific reduction of repressive H3K9me3 marks at promoters of mesenchymal genes, such as Calponin (CNN1), and genes involved in TGF-β signaling, such as AKT Serine/Threonine Kinase 3 (AKT3) and sulfatase 1 (SULF1). Silencing of JMJD2B prevented the EndMT-induced reduction of H3K9me3 marks at these promotors and further repressed these EndMT-related genes. Our study reveals that endothelial identity and function is critically controlled by the histone demethylase JMJD2B, which is induced by EndMT-promoting pro-inflammatory and hypoxic conditions and support the acquirement of a mesenchymal phenotype.
Publication Title
The histone demethylase JMJD2B regulates endothelial-to-mesenchymal transition.
Sample Metadata Fields
Age, Cell line, Treatment
View Samples- Homo sapiens
- 7 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
Impaired or excessive growth of endothelial cells contributes to several diseases. However, the functional involvement of regulatory long non-coding RNAs in these processes is not well defined. Here we show that the long non-coding antisense transcript of GATA6 (GATA6-AS) interacts with the epigenetic regulator LOXL2 to regulates endothelial gene expression via changes in histone methylation. Using RNA deep sequencing, we find that GATA6-AS is up-regulated in endothelial cells during hypoxia. Silencing of GATA6-AS diminishes TGF-2-induced endothelial-mesenchymal transition in vitro and promotes formation of blood vessels in mice. We identify LOXL2, known to remove activating H3K4me3 chromatin marks, as a GATA6-AS-associated protein, and reveal a set of angiogenesis-related genes that are inversely regulated by LOXL2 and GATA6-AS silencing. As GATA6-AS silencing reduces H3K4me3 methylation of two of these genes, periostin and cyclooxygenase-2, we conclude that GATA6-AS acts as negative regulator of nuclear LOXL2 function.
Publication Title
The lncRNA GATA6-AS epigenetically regulates endothelial gene expression via interaction with LOXL2.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
Impaired or excessive growth of endothelial cells contributes to several diseases. However, the functional involvement of regulatory long non-coding RNAs in these processes is not well defined. Here we show that the long non-coding antisense transcript of GATA6 (GATA6-AS) interacts with the epigenetic regulator LOXL2 to regulates endothelial gene expression via changes in histone methylation. Using RNA deep sequencing, we find that GATA6-AS is up-regulated in endothelial cells during hypoxia. Silencing of GATA6-AS diminishes TGF-2-induced endothelial-mesenchymal transition in vitro and promotes formation of blood vessels in mice. We identify LOXL2, known to remove activating H3K4me3 chromatin marks, as a GATA6-AS-associated protein, and reveal a set of angiogenesis-related genes that are inversely regulated by LOXL2 and GATA6-AS silencing. As GATA6-AS silencing reduces H3K4me3 methylation of two of these genes, periostin and cyclooxygenase-2, we conclude that GATA6-AS acts as negative regulator of nuclear LOXL2 function.
Publication Title
The lncRNA GATA6-AS epigenetically regulates endothelial gene expression via interaction with LOXL2.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
The adipose tissue is an endocrine regulator and a risk factor for atherosclerosis and cardiovascular disease when by excessive accumulation induces obesity. Although the adipose tissue is also a reservoir for stem cells (ASC) their function and stemcellness has been questioned. Our aim was to investigate the mechanisms by which obesity affects subcutaneous white adipose tissue (WAT) stem cells.
Publication Title
Stem cells isolated from adipose tissue of obese patients show changes in their transcriptomic profile that indicate loss in stemcellness and increased commitment to an adipocyte-like phenotype.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 56 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We previously generated genetically engineered mouse (GEM) models based on perturbation of Tp53, Rb with or without Brca1 or Brca2 that develop serous epithelial ovarian cancer (SEOC) closely resembling the human disease on histologic and molecular levels. We have adapted these GEM models to orthotopic allografts that uniformly develop tumors with short latency in immunocompetent recipients and are ideally suited for routine preclinical studies. To monitor passaged tumors at the molecular level, we analyzed transcriptional profiles of a set of primary SEOC and matching derived passaged tumors. We have merged this dataset with previously published ( doi: 10.1158/0008-5472.CAN-11-3834; PMID 22617326) dataset of murine primary ovarian tumors from our GEM models (GSE46169) and merged and compared them to expression profiles of human dataset published previously (doi: 10.1038/nature10166).
Publication Title
Pathway-specific engineered mouse allograft models functionally recapitulate human serous epithelial ovarian cancer.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 30 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
We have developed mouse models for serous epithelial ovarian cancer (SEOC) based on conditional inactivation of p53 and Rb tumor suppression (RB-TS) in combination with or without Brca1/2 following injection of adenovirus expressing Cre recombinase into the ovarian bursa. These models develop metastatic (Stage IV) disease with key histopathological features resembling human SEOC.To determine whether these mouse tumors resemble human SEOC at the molecular level, we conducted global gene expression analysis on 27 ovarian carcinomas and 3 pooled normal ovarian surface epithelium samples (single epithelial layer isolated from ovarian surface by laser capture).
Publication Title
Perturbation of Rb, p53, and Brca1 or Brca2 cooperate in inducing metastatic serous epithelial ovarian cancer.
Sample Metadata Fields
Specimen part
View Samples