Similar Datasets
Project description:The moderate response of smooth muscle cells is beneficial to the repair of vascular injury, while the continuous exposure of intravascular growth factors, and other stimulating factors will cause the dysfunction of smooth muscle cells, leading to the pathological remodeling of blood vessels, which is called neointimal hyperplasia. The aim of this study is to investigate the biological function of PTPN14 in vascular smooth muscle cells (VSMCs) and the mechanism of PTPN14 in regulating neointimal hyperplasia.
2024-07-17 | GSE267140 | GEO
Project description:Lung smooth muscle cells are including bronchiolar and vascular smooth muscle cells. In order to get adult lung smooth muscle cells, we use transgenic mouse line with smooth muscle actin creERT2, which is a transgenic cre recombinase in Acta2 (contractile smooth muscle cell gene). This mouse line also contains a CAG promoter-driven red fluorescent protein variant (tdTomato) - all inserted into the ROSA26 locus. This mouse line express robust tdTomato fluorescence following cre-mediated recombination after Tamoxifen injection.
2020-05-01 | GSE148008 | GEO
Project description:Loss of contractility and acquisition of an epithelial phenotype of vascular smooth muscle cells (VSMCs) are key events in proliferative vascular pathologies such as atherosclerosis and post-angioplastic restenosis. There is no proper cell culture system allowing VSMC differentiation so that it is difficult to delineate the molecular mechanism responsible for proliferative vasculopathy. We investigated whether a micro-patterned substrate could restore the contractile phenotype of VSMCs in vitro. To induce and maintain the differentiated VSMC phenotype in vitro, we introduced a micro-patterned groove substrate to modulate the morphology and function of VSMCs.
2013-11-14 | E-MTAB-1888 | biostudies-arrayexpress
Project description:We compared the global gene expression profiles of C57BL/6 mice aortas with the profiles of cultured vascular smooth muscle cells (vSMC) from the same mice, and determined whether gene responses to dioxin exposure in the vSMCs would be predictive of responses in the aorta.
2003-10-29 | E-MEXP-23 | biostudies-arrayexpress
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 SIRT6 in the regulation of VSMCs phenotype switch, we established mouse vascular smooth muscle cells in which each target gene has been knocked down by siRNA.
2024-12-11 | GSE246209 | GEO
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 EZH2 in the regulation of VSMCs phenotype switch, we established mouse vascular smooth muscle cells in which each target gene has been knocked down by siRNA.
2023-12-16 | GSE227177 | GEO
Project description:Gene expression profiling of miR-128 overexpression in Primary Mouse Vascular Smooth Muscle Cells (VSMCs)
| PRJNA513344 | ENA
Project description:MicroRNAs (miRNAs) are small non-coding RNAs that modulate gene expression by negatively regulating translation of target genes. miRNAs involvement in vascular smooth muscle cell (VSMC) biology has been deeply investigated, nevertheless the role of miR-128 in such context has not been yet explored. We aimed to evaluate whether this miR-128 might modulate VSMC phenotype similarly to what was previously observed for other type of contractile cells, such as cardiomyocytes (CM) and skeletal muscle cells. To this end, we compared the expression profiles of miR-128 overexpression in Primary mouse VSMCs and control groups (treated with scrambled miRNA). The expression profiles were defined by Illumina arrays.
2020-09-07 | GSE124764 | GEO
Project description:Transcriptional profiling of mouse VSMCs comparing control with VSMCs cultured with TNF-α Apoptosis of vascular smooth muscle cells (VSMCs) is a process that regulates vessel remodeling in various cardiovascular diseases. The specific mechanisms that control VSMC apoptosis remain unclear. The present study aimed to investigate whether microRNA-494 (miR-494) is involved in regulating VSMC apoptosis and its underlying mechanisms. Cell death ELISA and terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling assays were used to detect apoptosis of murine VSMCs following stimulation with tumor necrosis factor(TNF-α). The results indicated that TNF-α-upregulated VSMC apoptosis in a dose-dependent manner. Microarray analysis was used to evaluate the expression profile of microRNAs following TNF-α-stimulation in murine VSMCs. The expression of miR-494 was downregulated, whereas B-cell lymphoma 2-like 11 (BCL2L11) protein expression levels were upregulated in VSMCs following treatment with TNF- . Luciferase reporter assays confirmed that BCL2L11 was a direct target of miR-494. Transfection with miR-494 mimics decreased VSMC apoptosis and downregulated BCL2L11 protein levels. Conversely, transfection with miR-494 inhibitors increased cell apoptosis and upregulated BCL2L11 protein levels, suggesting that miR-494 may function as an essential regulator of BCL2L11. The increase in apoptosis caused by miR-494 inhibitors was abolished in cells co-transfected with BCL2L11-targeting small interfering RNA. The findings of the present study revealed that miR-494 inhibited TNF-α-induced VSMC apoptosis by downregulating the expression of BCL2L11.
2019-02-28 | GSE127016 | GEO
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.
2020-03-01 | GSE140947 | GEO