Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE211720 | GEO | 2022/09/18

REPOSITORIES: GEO

ACCESS DATA

Json Xml

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

miRNA-sequencing of human non-calcificated and calcificated aortic valve interstitial cells

Project description:To explore the miR expression profile of calcified valve interstitial cells (VICs) induced by high calcium/phosphate, identify the key miRNA in the calcification process of VICs, and probe effect of miRs in regulating valve calcification.

2022-12-26 | GSE221671 | GEO

Vitamin D sterol effects on coronary ASMC genes

2008-06-28 | GSE11917 | GEO

mRNA expression profile in vascular smooth muscle cells (VSMCs) after inducing calcification

Project description:Vascular calcification (VC) is often associated with cardiovascular and metabolic diseases. However, the molecular mechanisms linking VC to these diseases have yet to be elucidated. Here we report that MDM2-induced polyubiquitination of histone deacetylase 1 (HDAC1) mediates VC. Loss of HDAC1 activity via either chemical inhibitor or genetic ablation enhanced VC. HDAC1 protein, but not mRNA, was reduced in cell and animal calcification models and in human calcified coronary artery. In the calcification-provoking condition, proteasomal degradation of HDAC1 preceded VC. The calcification-provoking condition induced MDM2 E3 ligase, which then resulted in HDAC1 K74 polyubiquitination. Overexpression of MDM2 enhanced VC, whereas loss of MDM2 blunted it. Decoy peptides spanning HDAC1 K74 and RG 7112, an MDM2 inhibitor, prevented VC in vivo and in vitro. These results demonstrate a previously unknown ubiquitination pathway and suggest MDM2-mediated HDAC1 polyubiquitination as a new therapeutic target in VC. Calcification was induced in rat aorta vascular smooth muscle cells with inorganic phosphate (Pi). Total RNA were extracted from the cells 3 and 6 days later. mRNA profile of the sample was compared with normal control.

2015-11-07 | E-GEOD-74755 | biostudies-arrayexpress

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

CKD-PROTEOME project, namely Calciprotein particle-activated endothelial cells exhibit altered mitochondria related to calcium dysregulation

Project description:Chronic kidney disease (CKD) is associated with increased cardiovascular risk, morphologically characterized by vascular calcification (VC). In CKD, high serum phosphate levels result in enhanced calcification propensity and the formation of circulating crystalline nanoaggregates (calciprotein particles, CPP2) containing calcium, phosphate and serum proteins. CPP2 can induce VC directly and this is recapitulated in vascular smooth muscle cells (VSMCs) in vitro. Under physiological conditions, vascular endothelial cells (ECs), rather than VSMCs are primarily exposed to circulating CPP2. Knowledge on the modulating effects of ECs on VC development is still in its infancy. The aim of this study was to investigate the calcium and bioenergetics signaling in CPP2-induced EC, including using ECs global proteome.

2024-02-06 | PXD049245 | iProX

Impact of high-phosphate diet on aortic gene expression

Project description:Uremic media calcification is not only driven by systemic factors such as hyperphosphatemia, but also crticially dependent on vascular smooth muscle cells per se. We hypothesized that the different developmental origins of vscular smooth muscle cells might lead to a heterogeneous susceptibility to develop media calcification. Upon high-phosphate diet, the transcriptional profile revealed an induction of an inflammatory vascular smooth muscle phenotype only in the abdominal, but not in the thoracic aorta. Thus, smooth muscle cells from different lineages responded differently to morphogenetic cues in vivo. We analyzed 3-4 replicates of the thoracic and abdominal aorta, which were previously exposed to either high-phosphate diet (HPD) or standard chow diet (SCD), respectively.

2014-05-26 | E-GEOD-57818 | biostudies-arrayexpress

LncRNA expression profile and target gene prediction of calcification in human aortic smooth muscle cells induced by DPP4

Project description:Arterial media calcification caused by diabetes is an important cause of vascular calcification. Dipeptidyl peptidase-4 (DPP4) is associated with diabetic arterial media calcification. At the same time, long non-coding RNA(lncRNA) is closely related to the evolution of a variety of cardiovascular diseases, but the involvement of lncRNA in vascular calcification induced by DPP4 has not been reported in details. In this study, we established a model of human aortic smooth muscle cells (HASMCs) calcification induced by DPP4. There was a significant difference in the expression of lncRNAs and mRNAs between normal and calcified vascular smooth muscle cells detected by gene chip technology. Based on the results of microarray detection, we found that lncRNA may be involved in vascular calcification induced by DPP4 through regulating target genes.

2021-12-03 | GSE189923 | GEO

Impact of high-phosphate diet on aortic gene expression

2014-05-26 | GSE57818 | GEO

Decoding the transcriptome of calcified atherosclerotic plaque at single-cell resolution

Project description:Atherogenesis involves an interplay of inflammation, tissue remodeling and cellular transdifferentiation (CTD), making it especially difficult to precisely delineate its pathophysiology. Here we examine the single-cell transcriptome of entire calcified atherosclerotic core (AC) plaques and patient-matched proximal adjacent (PA) portions of carotid artery tissue from patients undergoing carotid endarterectomy. We use a novel tissue dissociation strategy, single-cell RNA sequencing, and systems-biology approaches to analyze the transcriptional profiles of six main cell populations and identify key gene drivers of pathogenic biological processes in vascular smooth muscle cells (VSMCs) and endothelial cells (ECs).

2020-10-21 | GSE159677 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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