Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profile of TGFbeta treated human coronary smooth muscle cell (HCASM)

ABSTRACT: TGFbeta induces VSMC gene expression in human coronary artery smooth muscle cell (HCASM)

ORGANISM(S): Homo sapiens

PROVIDER: GSE85910 | GEO | 2017/03/08

SECONDARY ACCESSION(S): PRJNA339734

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptional profiling of osteogenic medium calcified human primary coronary artery smooth muscle cells.

Project description:Transcriptomics analysis of human coronary artery smooth muscle cells cultured in osteogenic medium (OM) to induce a mineralized extracellular matrix. To study the underlying molecular mechanisms driving vascular calcification, we analyzed the transcriptome of osteogenic medium (OM)-calcified human coronary artery smooth muscle cells on day 7.

2022-09-18 | GSE211722 | GEO

Transcriptome sequencing of human coronary artery smooth muscle cell under treatment of nitrated fatty acid

Project description:RNA-seq profiling of human coronary artery smooth muscle cells under treatment of nitrated conjugated linoleic acids (NO2-CLA)

2018-05-31 | GSE100676 | GEO

Long read sequencing of nuclear RNAs from human coronary artery smooth muscle cells

Project description:To study isoforms of nuclear RNAs, including CARMN lncRNA, we performed Oxford Nanopore long-read sequencing of RNAs isolated from the nuclear fraction of human coronary artery smooth muscle cells.

2021-04-06 | GSE165445 | GEO

Transcriptional profiling of calcium-phosphate calcified human primary coronary artery smooth muscle cells.

Project description:Transcriptomics analysis of human coronary artery smooth muscle cells cultured in calcium-phosphate medium (CaP) to induce a mineralized extracellular matrix. To study the underlying molecular mechanisms driving vascular calcification, we analyzed the transcriptome of calcium-phosphate calcified human cronary aortic smooth muscle cells on day 3.

2022-09-18 | GSE211720 | GEO

Transcription profiling of human coronary artery smooth muscle treated with vitamin D sterol

Project description:Chondro/osteoblastic and cardiovascular-disease associated genes are modulated in human coronary artery smooth muscle cells that calcify in the presence of phosphate and vitamin D sterols. Looking at the effect of media conditions with and without Vitamin D, paracalcitriol (a vitamin D analog), or R568 (a calcimimetic) vs. dose and time on calcification of human coronary smooth muscle cells. Experiment Overall Design: CASMCs were exposed to differentiation medium [beta glycerophosphate (10 mM), ascorbic acid (50 mg/ml), and dexamethasone (10-9 M) with and without calcitriol or paricalcitol (10-8 M) for 7 days, and total RNA was examined by microarray.

2008-10-21 | E-GEOD-11917 | biostudies-arrayexpress

Overexpression of Transcription Factor GATA6 in Human Coronary Artery Smooth Muscle Cells in vitro

Project description:Vascular smooth muscle cell plasticity plays a pivotal role in the pathophysiology of vascular diseases. Despite compelling evidence demonstrating the importance of transcription factor GATA6 in vascular smooth muscle, the functional role of GATA6 remains poorly understood. The aim of this study was to elucidate the role of GATA6 on cell migration and to gain insight into GATA6-sensitive genes in smooth muscle. Therefore, we performed Affymetrix microarray analysis on human coronary artery smooth muscle cells after overexpressing GATA6 by adenovirus transduction and compared it to control which are cell transduced with Ad-CMV-null.

2022-10-31 | GSE216686 | GEO

UHRF1-mediated epigenetic regulation of smooth muscle cell modulates development of vascular pathologies

Project description:Adult vascular smooth muscle cells (VSMCs) dedifferentiate in response to extracellular cues such as vascular damage and inflammation. Dedifferentiated VSMCs are proliferative, migratory, less contractile, and can contribute to vascular repair as well as to cardiovascular pathologies such as intimal hyperplasia/restenosis in coronary artery and arterial aneurysm. We here demonstrate the role of ubiquitin-like containing PHD and RING finger domains 1 (UHRF1) as an epigenetic master regulator of VSMC plasticity. UHRF1 expression correlated with the development of vascular pathologies associated with modulation of noncoding RNAs, such as microRNAs. miR-145 — pivotal in regulating VSMC plasticity, which is reduced in vascular diseases — was found to control Uhrf1 mRNA translation. In turn, UHRF1 triggered VSMC proliferation, directly repressing promoters of cell-cycle inhibitor genes (including p21 and p27) and key prodifferentiation genes via the methylation of DNA and histones. Local vascular viral delivery of Uhrf1 shRNAs or Uhrf1 VSMC-specific deletion prevented intimal hyperplasia in mouse carotid artery and decreased vessel damage in a mouse model of aortic aneurysm. Our study demonstrates the fundamental role of Uhrf1 in regulating VSMC phenotype by promoting proliferation and dedifferentiation. UHRF1 targeting may hold therapeutic potential in vascular pathologies.

2018-12-05 | GSE99472 | GEO

Quantitative trait loci mapped for TCF21 binding, chromatin accessibility and chromosomal looping in coronary artery smooth muscle cells reveal molecular mechanisms of coronary disease loci

Project description:To better understand the fundamental molecular mechanisms that contribute to complex human diseases such as coronary artery disease (CAD), we have created a catalog of genetic variants associated with three stages of transcriptional cis-regulation in primary human coronary artery vascular smooth muscle cells. To this end, we used a pooling approach to map quantitative trait locus associations (QTLs) for TCF21 binding (ChIPseq), chromatin accessibility (ATACseq), and chromosomal looping (HiC). We find significant overlap of these QTLs, and several analyses indicate their relationship to smooth muscle specific genes, the binding of smooth muscle transcription factors, and enrichment in CAD-associated loci. These QTLs are extensively validated and allele-specific chromatin looping at the FN1 disease locus is shown to be mediated by activation of the CAD-associated TGFb1 pathway. In sum, these results uncover thousands of loci affecting cis-regulation in a key cell type for CAD, including many that may contribute to CAD risk.

2020-05-07 | GSE141752 | GEO

Quantitative trait loci mapped for TCF21 binding, chromatin accessibility and chromosomal looping in coronary artery smooth muscle cells reveal molecular mechanisms of coronary disease loci [array]

2020-05-12 | GSE150403 | GEO

Quantitative trait loci mapped for TCF21 binding, chromatin accessibility and chromosomal looping in coronary artery smooth muscle cells reveal molecular mechanisms of coronary disease loci (ChIP-Seq)

2020-05-07 | GSE141751 | GEO