Combinatorial role of Jmjd2b and Jmjd2c in mESC identity
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ABSTRACT:
PROVIDER: PRJNA185046 | ENA |
REPOSITORIES: ENA
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Project description:Genome-wide occupancy of biotinylated Jmjd2b, Jmjd2c from mESCs, as well as occupancy of selected factors and histone marks from wild-type mESCs, Anti-GFP KD, Jmj2b KD and Jmjd2c KD mESCs genome To identify genome-wide binding target sites of Jmjd2b and Jmjd2c in the mESCs genome, and genome-wide binding sites for selected factors and histone marks from Anti-GFP KD, Jmjd2b KD and Jmjd2c KD mESCs
2013-12-01 | E-GEOD-43229 | biostudies-arrayexpress
Project description:Genome-wide occupancy of biotinylated Jmjd2b, Jmjd2c from mESCs, as well as occupancy of selected factors and histone marks from wild-type mESCs, Anti-GFP KD, Jmj2b KD and Jmjd2c KD mESCs genome
2013-12-01 | GSE43229 | GEO
Project description:We used microarray to determine the changes in gene expression profile after KD of Jmjd2b and Jmjd2c compared to Anti-GFP KD from mES cells Mouse ES cells were infected with AntiGFP, Jmjd2b and Jmjd2c shRNAs lentivirus, puromycin selected, passage them 2-3 times, collected for RNA isolation and gene expression
2013-12-01 | E-GEOD-43059 | biostudies-arrayexpress
Project description:We used microarray to determine the changes in gene expression profile after KD of Jmjd2b and Jmjd2c compared to Anti-GFP KD from mES cells
2013-12-01 | GSE43059 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2013-12-01 | E-GEOD-43231 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below.
2013-12-01 | GSE43231 | GEO
Project description:Combinatorial role of Jmjd2b and Jmjd2c in mESCs identity
| PRJNA185048 | ENA
Project 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.
2020-01-08 | GSE143148 | GEO
Project 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.
2020-01-08 | GSE143150 | GEO