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Endothelial to Mesenchymal Transition

ABSTRACT: Driving HUVECs toward mesenchymal fate

ORGANISM(S): Homo sapiens

PROVIDER: GSE56309 | GEO | 2016/04/05

SECONDARY ACCESSION(S): PRJNA242886

REPOSITORIES: GEO

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Endothelial to Mesenchymal Transition

Project description:Driving HUVECs toward mesenchymal fate Comparison of untreated HUVECs, HUVECs treated with TGF-B, HUVECS treated with TGF-B and oxidative stress, and comparator human dermal fibroblasts

2016-04-05 | E-GEOD-56309 | biostudies-arrayexpress

Acetate controls endothelial-to-mesenchymal transition during atherosclerosis [2]

Project description:To investigate the gene expression profiling during endothelial-to-mesenchymal transition , and identify the main changes in metaboltic and EndoMT related genes.

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Project description:To investigate the gene expression profiling during endothelial-to-mesenchymal transition , and identify the main changes in metaboltic and EndoMT related genes.

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Analysis of Gene Expression changes in human intestinal endothelial-to-mesenchymal transition

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The histone demethylase JMJD2B regulates endothelial-to-mesenchymal transition [microarray]

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

The histone demethylase JMJD2B regulates endothelial-to-mesenchymal transition [HTS]

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Transcriptome profiling of human endothelial cells undergoing endothelial-to-mesenchymal transition

Project description:To investigate the transcriptome of endothelial cells undergoing endothelial-to-mesenchymal transition, transcription profiling was performed on primary human endothelial cells in the presence or absence of 40mM acetate following control or cytokine treatment for 4 days. We then performed gene expression profiling analysis using data obtained from RNA-seq of primary human endothelial cells.

2023-10-16 | GSE236730 | GEO

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Time course of TGFbeta induced epithelial mesenchymal transition (EMT) in H358 NSCLC cells.

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2019-01-23 | GSE125365 | GEO

Multiomic profiling of in vitro models of endothelial-to-mesenchymal transition reveals endothelial cell subtype is a major determinant of fidelity to observed states in atherosclerosis

Project description:Endothelial-to-mesenchymal transition (EndMT) is an example of endothelial cell (EC) heterogeneity which is commonly modeled in vitro to better understand driving mechanisms of disease proceses, including atherosclerosis. We used multi-modal single nucleus RNA sequencing (snRNA-seq) and ATAC sequencing (snATAC-seq) to analyze the diversity of ECs in vitro, divergent EC responses to known EndMT perturbations, and the ability of in vitro EC known EndMT models to recapitulate the in vivo 'omic profiles of cells observed in atherosclerosis.

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