Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE118815 | GEO | 2020/12/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptome changes during Endothelial to Mesenchymal Transition (EndMT) using a TGF-b2 and IL-1b in vitro model of EndMT in HUVEC and HPAEC

Project description:Endothelial-to-mesenchymal transition (EndMT) is a dynamic transformation process that has a functional impact upon pathological vascular remodelling. However, the molecular mechanisms that govern EndMT remain largely unknown. We modelled this process in vitro by exposing human primary endothelial cells to a combination of transforming growth factor-β2 (TGF- β2) and interleukin-1β (IL-1β). RNAseq was carried out to analyse the change of gene expression during the transition and define the transcriptional architecture of EndMT.

2020-12-31 | GSE118446 | GEO

Expression Analysis between HUVECs and EndMTed HUVECs

Project description:Prostate cancer often progresses to castration-resistant prostate cancer (CRPC), with neuroendocrine prostate cancer (NEPC) representing a highly aggressive variant. This study shows that endothelial-to-mesenchymal transition (EndMT) in vascular endothelial cells, induced by IL-1β and TGF-β2, enhances neuroendocrine differentiation in prostate cancer cells. LNCaP cells co-cultured with EndMTed HUVECs exhibited increased expression of neuroendocrine markers such as chromogranin A. GM-CSF emerged as a key mediator in this process, and its addition under androgen deprivation conditions further elevated neuroendocrine marker expression. Anti-androgen therapy with enzalutamide also paradoxically increased IL-1β and TGF-β2 secretion, promoting EndMT and subsequent neuroendocrine differentiation. These results highlight the potential of targeting EndMT and GM-CSF pathways as therapeutic strategies for aggressive, treatment-resistant forms of NEPC.

2024-11-28 | GSE281995 | GEO

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

Single cell RNA-seq analysis of endothelial cells (HUVEC) treated with IL1b and TGFb2 as a model of endothelial to mesenchymal transition (EndMT)

Project description:Endothelial-to-mesenchymal transition (EndMT) is a dynamic biological process involved in pathological vascular remodeling. However, the molecular mechanisms that govern this transition remain largely unknown. To study EndMT in vitro, human umbilical vein endothelial cells (HUVEC) were treated with transforming growth factor-β2 and interleukin-1β, leading to a decrease of endothelial markers as well as an increase of mesenchymal markers and EndMT regulators after 7 days. Single-cell RNA-seq was carried out to study the dynamics of the transition.

2021-04-06 | GSE159843 | GEO

Gene expression changes between naïve and IL-1β + TGF-β2 dual cytokine licensed equine mesenchymal stem cells

Project description:The study objectives were to 1) determine mesenchymal stem cell (MSC) surface expression of major histocompatibility complex (MHC) class I and transcriptome-wide gene expression changes following IL-1β + TGF-β2 dual licensing and 2) evaluate if IL-1β + TGF-β2 dual licensed MSCs had greater ability to positively modulate tenocyte function compared to naïve MSCs.

2024-02-25 | GSE256139 | 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

MiR-181b Targets Semaphorin 3a to Mediate TGF-β-induced Endothelial to Mesenchymal Transition: Implication in Atrial Fibrillation

Project description:Background:This study investigated if and how atrial endothelial cells may transform to mesenchymal cells and contribute to atrial fibrosis via endothelial-to-mesenchymal transition (EndMT). Results:We show a novel mechanistic link between TGF-β1/SMAD signaling and decreased Sema3a expression through the induction of miR-181b; this pathway plays an important role in EndMT associated with the pathogenesis of AF. Both miR-181b and Sema3a are potential therapeutic targets in AF.

2022-04-13 | GSE156835 | GEO

MiR-181b targets semaphorin 3a to mediate TGF-β-induced endothelial-to-mesenchymal transition related to atrial fibrillation

2022-04-27 | GSE201318 | 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.

2023-05-03 | GSE228428 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data