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Long non-coding RNA MIR503HG controls endothelial-to-mesenchymal transition

ABSTRACT: Long non-coding RNA MIR503HG controls endothelial-to-mesenchymal transition

PROVIDER: PRJNA486849 | ENA |

REPOSITORIES: ENA

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Long non-coding RNA MIR503HG controls endothelial-to-mesenchymal transition

Project description:Endothelial-to-mesenchymal transition (EndMT) is a dynamic transformation process that has a functional impact upon pathological vascular remodelling. The molecular mechanisms that govern EndMT remain largely unknown. By induction of EndMT in human primary endothelial cells (EC), using a combination of transforming growth factor-β2 (TGF-b2) and interleukin-1b (IL-1β), we identified the dramatic loss of the lncRNA MIR503HG, as a common signature across multiple primary EC types. Targeted depletion of MIR503HG spontaneously induced EndMT. Overexpression of MIR503HG repressed EndMT despite TGF-β2 and IL-1β co-stimulation. RNA-seq was carried out to identify the changes in gene expression induced by MIR503HG overexpression. We showed that over 25% of the EndMT-transcriptome signature was inhibited upon MIR503HG overexpression. Crucially, phenotypic changes induced by MIR503HG were independent of the functional regulation of miR-503 and miR-424, both harbored within the MIR503HG locus. Collectively, we identify the lncRNA MIR503HG as an essential regulator of EndMT.

2020-12-31 | GSE118815 | GEO

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.

2023-05-01 | GSE224939 | GEO

Acetate controls endothelial-to-mesenchymal transition during atherosclerosis [1]

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

2023-05-01 | GSE224907 | GEO

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

Project description:This SuperSeries is composed of the following subset Series: GSE15933: Analysis of Gene Expression changes in human intestinal endothelial-to-mesenchymal transition - UNTREATED/CONTROL GROUP GSE15934: Analysis of Gene Expression changes in human intestinal endothelial-to-mesenchymal transition - TRANSFORMED GROUP Refer to individual Series

2011-11-02 | E-GEOD-15975 | biostudies-arrayexpress

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

The histone demethylase JMJD2B regulates endothelial-to-mesenchymal transition

Project description:The histone demethylase JMJD2B regulates endothelial-to-mesenchymal transition

| PRJNA599370 | ENA

ARPCs Can Revert Lps-Induced Endothelial-to-Mesenchymal Transition of Endothelial Cells

Project description:ARPCs Can Revert Lps-Induced Endothelial-to-Mesenchymal Transition of Endothelial Cells

| PRJNA480439 | ENA

Endothelial Cells from different anatomical origin have distinct responses during Snail/TGF-β2-mediated Endothelial-Mesenchymal Transition

Project description:Endothelial-mesenchymal transition (EndMT) is a complex process, in which differentiated endothelial cells undergo phenotypic transition to mesenchymal cells. Given the diversity of the vascular system in architecture, structure, and embryonic origins, it is not clear if endothelial cells lining different vessels are able to undergo EndMT. Therefore, the aim of this study was to evaluate the molecular and functional changes that occur in different types of endothelial cells after induction of EndMT through overexpression of Snail and TGF-β2. Different types of endothelial cells (human umbilical vein, heart, and lung) have distinct response when induced to undergo EndMT. Coronary artery endothelial cells (HCAEC) induced with combined Snail overexpression plus TGF-β2 treatment promotes a decrease of endothelial markers, an increase of mesenchymal markers and migration. The mechanism that HCAEC undergoing EndMT may be mediated through Notch and non-canonical Wnt signaling pathways. These results provide the foundation for understanding the roles of specific signaling pathways in mediating EndMT in endothelial cells from different anatomical origin.

2017-04-22 | GSE96089 | GEO

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]

2020-01-08 | GSE143148 | GEO

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