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Genome-wide analysis of genes induced by thrombin at 2 hour and 8 hour in human aortic smooth muscle cells

ABSTRACT: Genome-wide analysis of genes induced by thrombin at 2 hour and 8 hour in human aortic smooth muscle cells

PROVIDER: PRJNA412856 | ENA |

REPOSITORIES: ENA

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Genome-wide analysis of genes induced by thrombin at 2 hour and 8 hour in human aortic smooth muscle cells

Project description:Human aortic smooth muscles are quiesced for 24 hours followed by treatment with thrombin for 2 hours and 8 hours in presence or absence of cyclosporin A (10 micromolar) to analyze the effect of thrombin on expression pattern of various genes in presence of cyclosporin A.

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Transcription profiling of rat thrombin-stimulated vascular smooth muscle cells

Project description:The strength and duration of extracellular signal-regulated kinases 1/2 (ERK1/2) phosphorylation can define the phenotypic outcome of cells. Stimualtion of the proteinase-activated receptor (Par) triggers a Gi-dependent long-lasting transactivation of the epidermal growth factor receptor and subsequent ERK1/2 phosphorylation. To understand the mechnaisms underlying this signaling cascade, microarray analysis was performed in vascular smooth muscle cells. Experiment Overall Design: Par receptors on neonatal rat aortic smooth muscle cells were stimulated with thrombin or TRAP in presence or abscence of Gi-uncoupling pertussis toxin.

2009-05-02 | E-GEOD-15841 | biostudies-arrayexpress

Smooth muscle cell reprogramming in aortic aneurysms [RNA-Seq]

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Project description:Smooth muscle cell reprogramming in aortic aneurysms

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Effect of IL-1b treatment on cultured rat aortic smooth muscle cells

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Silencing of STE20-Type Kinase STK25 in Human Aortic Endothelial and Smooth Muscle Cells is Atheroprotective

Project description:Recent studies highlight the importance of lipotoxic damage in aortic cells as the major pathogenetic contributor of atherosclerotic disease. Since the STE20-type kinase STK25 has been shown to exacerbate ectopic lipid storage and associated cell injury in several metabolic organs, we here investigated its role in the main cell types of vasculature. We depleted STK25 by small interfering RNA in human aortic endothelial and smooth muscle cells exposed to oleic acid and oxidized LDL. In both cell types, the silencing of STK25 reduced lipid accumulation and suppressed activation of inflammatory and fibrotic pathways as well as lowered oxidative and endoplasmic reticulum stress. Notably, in smooth muscle cells, STK25 inactivation hindered the shift from a contractile to a synthetic phenotype. Together, we provide the first evidence that antagonizing STK25 signaling in human aortic endothelial and smooth muscle cells is atheroprotective, highlighting this kinase as a new potential therapeutic target for atherosclerotic disease.

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scRNA-seq of lineage traced mouse aortic smooth muscle cells with cell Hashing

Project description:scRNA-seq of lineage traced mouse aortic smooth muscle cells with cell Hashing

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Expression anaysis of mouse aortic vascular smooth muscle cells

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