Project description:We sought to identify microRNAs that were differentially regulated in cultured primary human aortic smooth muscle cells (SMCs) when exposed to growth arrest via serum starvation over two time points - 48 hours and 72 hours, when compared with serum-fed cells. This treatment leads to increased expression of SMC differentiation markers such as ACTA2, MYH11 and TAGLN. We identified 31 significantly regulated miRNA candidates during this process, 28 rising and 3 falling. Human aortic SMCs (AoSMCs) were propagated in growth media. Control plates were harvested, and the remaining plates were serum starved for 48 (SS48) or 72 hours (SS72) in serum-free basal media. Several arrays were excluded from final analysis after QC, resulting in a final set of 10.
Project description:Transcriptional profiling of human aortic smooth muscle cells (HSMCs) comparing exposed with nicotine or not. Two-condition experiment, control vs. treated HSMCs by nicotine.
Project description:Primary human aortic smooth muscle cells (HAoSMC) were starved over night in 1% FCS. On the next day cells were treated with 100nM Anandamide (AEA) or EtOH as control for 4h in presence of 10µM diclofenac. Subsequently cells were treated with or without 10ng/mL IL-1β for last 1.5h.
Project description:We used NGS-derived transcriptome profiling (RNA-seq) to compare the transcriptional difference between human aortic smooth muscle cells (HASMCs) infected with 20MOI adenovirus encoding human BAF60a (AdBAF60a) or GFP (AdGFP)
Project description:We used NGS-derived transcriptome profiling (RNA-seq) to compare the transcriptional difference between human aortic smooth muscle cells (HASMCs) transfected with 30nM siRNA targeting BAF60a (siBAF60a) or non-targeting siRNA (siControl)
Project description:Smooth muscle cell TGFβ signaling is one of the primary drivers of smooth muscle cell maturation. Inhibition of smooth muscle cell TGFβ signaling in hyperlipidemic mice induces vessel wall inflammation and vessel wall dilation/dissection and leads aortic aneurysm. We performed bulk RNAseq method to examine smooth muscle cell gene expression profile using fresh human tissues from normal aortic media smooth muscle cells and aneurysm aortic media smooth muscle cells.
Project description:Vascular smooth muscle cells (VSMCs) phenotype switch has been thought to be critical to the development of thoracic aneurysm/dissection. To investigate the function HDAC9 in the regulation of VSMCs phenotype switch, we used siRNA knockdown of HDAC9 in human aortic smooth muscle cells (HASMC)we established Human aortic smooth muscle cells (HASMCs).
Project description:Effects of TRPC1 silencing on whole-transcriptome gene expression were determined in human primary aortic vascular smooth muscle cells using whole-transcriptome gene expression profiling.
