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Effect of TGF-B treatment on human vascular smooth muscle cells

ABSTRACT: The authors did a microarray analysis to investigate the effect of TGF-B treatment on cultured smooth muscle cells from the human aorta. In particular, the authors were interested to see which cell types were upregulated or downregulated after treatment with TGF-B.

ORGANISM(S): Homo sapiens

PROVIDER: GSE30004 | GEO | 2011/06/16

SECONDARY ACCESSION(S): PRJNA143675

REPOSITORIES: GEO

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Effect of TGF-B treatment on human vascular smooth muscle cells

Project description:The authors did a microarray analysis to investigate the effect of TGF-B treatment on cultured smooth muscle cells from the human aorta. In particular, the authors were interested to see which cell types were upregulated or downregulated after treatment with TGF-B. Human Smooth muscle cells from 4 different donors in triplicates were analyzed. The cells were either untreated (n=12) or were treated with TGF-B (1 ng/ml)

2011-06-16 | E-GEOD-30004 | biostudies-arrayexpress

TGF-Î²/Smad3 Stimulates Stem Cell/Developmental Gene Expression and Vascular Smooth Muscle Cell De-Differentiation

Project description:In order to determine a mechanism through which TGF-b/Smad3 promote these effects, Affymetrix gene expression arrays were performed on primary rat SMCs infected with Smad3 and stimulated with TGF-b or infected with GFP alone. More than 200 genes were differentially expressed (>2.0 fold change, p<0.05) in TGF-b/Smad3 stimulated SMCs. We then performed GO term enrichment analysis using the DAVID bioinformatics database and found that TGF-b/Smad3 activated the expression of multiple genes related to either development or cell differentiation, several of which have been shown to be associated with multipotent stem or progenitor cells. Vascular smooth muscle cells from 3 rats were infected with adenovirus expressing Smad3 and treated with TGF-B for 24 h (TGF-B/Smad3 group). Adenovirus expressing GFP (GFP group) was control. TGF-B/Smad3 treated or control cells were used for RNA extraction and hybridization on Affymetrix microarrays (n=3).

2014-02-04 | E-GEOD-54624 | biostudies-arrayexpress

Vascular smooth muscle cell senescence instigates thoracic aortic aneurysm

Project description:In this study, we identified various cell clusters in human normal/sporadic TAA ascending aorta samples by single-cell RNA sequencing (scRNA-seq), and discovered the senescent vascular smooth muscle cells (VSMCs) significantly increased in TAA samples. Then we explored the molecular basis of TAA progression, and recognized the key regulators and pathways involved in the TAA progression regulation.

2023-12-01 | GSE143921 | GEO

PRDM16 Deficiency in Vascular Smooth Muscle Cells Aggravates Abdominal Aortic Aneurysm

Project description:Abdominal aortic aneurysm (AAA) is usually asymptomatic until life-threatening complications occur, predominantly involving aortic rupture. Currently, no drug-based treatments are available, primarily due to limited understanding of AAA pathogenesis. The transcriptional regulator PR domain–containing protein 16 (PRDM16) is highly expressed in the aorta, but its functions in the aorta are largely unknown. By RNA-seq analysis, we found that vascular smooth muscle cell–specific (VSMC-specific) Prdm16-knockout (Prdm16SMKO) mice already showed extensive changes in the expression of genes associated with extracellular matrix (ECM) remodeling and inflammation in the abdominal aorta under normal housing conditions without any pathological stimuli. Human AAA lesions displayed lower PRDM16 expression. Periadventitial elastase application to the suprarenal region of the abdominal aorta aggravated AAA formation in Prdm16SMKO mice. During AAA development, VSMCs undergo apoptosis because of both intrinsic and environmental changes, including inflammation and ECM remodeling. Prdm16 deficiency promoted inflammation and apoptosis in VSMCs. A disintegrin and metalloproteinase 12 (ADAM12) is a gelatinase that can degrade various ECMs. We found that ADAM12 is a target of transcriptional repression by PRDM16. Adam12 knockdown reversed VSMC apoptosis induced by Prdm16 deficiency. Our study demonstrated that PRDM16 deficiency in VSMCs promoted ADAM12 expression and aggravates AAA formation, which may provide potential targets for AAA treatment.

2023-06-08 | GSE222440 | GEO

Angiotensin II regulated gene expression in rat primary vascular smooth muscle cells (VSMC)

Project description:Atherosclerosis is one of the causative factors leading to the development of cardiovascular disease. Angiotensin II (AngII) is implicated in the pathological processes underlying atherosclerosis. We investigated the AngII regulated gene expression in primary vascular smooth muscle cells (VSMC). VSMCs were isolated from the thoracic aorta of male Wistar rats. Serum deprived VSMCs were stimulated with 100 nM AngII or vehicle for 2 hours, then RNA-Sequencing was carried out.

2022-07-03 | E-MTAB-11863 | biostudies-arrayexpress

The effect of Schisandra chinensis fruit extract (SCE) and Schisandrin B (SchB) on gene expression profile in TGF-β1-treated A7r5 rat aortic smooth muscle cell

Project description:Schisandra chinensis fruit extract (SCE) and its active ingredient Schisandrin B (SchB), which are effective in the treatment of vascular diseases, have been known to suppress transforming growth factor β1 (TGF-β1)-mediated Smad activation and myosin light chain (MLC) phosphorylation in vascular smooth muscle cells (VSMCs). However, it is still largely unknown about the pharmacologic effects and mechanisms of SCE and SchB on TGF-β1-induced intracellular signaling pathways in vascular smooth muscle cells (VSMCs).

2017-12-20 | GSE87439 | GEO

Smooth muscle cell mineralocorticoid receptor regulation of vascular microRNAs with aging

Project description:We used a smooth muscle cell-specific mineralocorticoid receptor knockout mouse to generate young and aged MR-intact and SMC-MR-KO aortic miRNA to examine the effect of age on vascular miRNA alterations in the presence and absence of SMC-MR. For more information about the mouse model see: McCurley, A et al. Direct regulation of blood pressure by smooth muscle cell mineralocorticoid receptors. Nat Med. 2012 Sep;18(9):1429-33

2016-07-29 | GSE84960 | GEO

Smooth muscle cell mineralocorticoid receptor regulation of vascular mRNAs with aging

Project description:We used a smooth muscle cell-specific mineralocorticoid receptor knockout mouse to generate young and aged MR-intact and SMC-MR-KO aortic mRNA to examine the effect of age on vascular mRNA alterations in the presence and absence of SMC-MR. For more information about the mouse model see: McCurley, A et al. Direct regulation of blood pressure by smooth muscle cell mineralocorticoid receptors. Nat Med. 2012 Sep;18(9):1429-33

2017-08-10 | GSE102397 | GEO

Effect of PDGF, TGF-β and miR-221 on gene expression during proliferation and differentiation of human aortic smooth muscle cells

Project description:To investigate the key molecular and mechanism during the proliferation and differentiation of human aortic smooth muscle cells, we treated HASMC cell lines with PDGF, TGF-β and miR-221.We then performed gene expression profiling analysis using data obtained from ONT long-read RNA-seq of 4 different treatment.

2023-10-12 | GSE209739 | GEO

NMuMG cell response to TGF-beta and TGF-beta +2APB treatments

Project description:Recent studies demonstrate that Ca2+ signaling has an important role in EMT. Use of Ca2+ blockers such as 2APB can inhibit cell migration induced by TGF-β. Interestingly, we see an unexpected increase in Snail expression upon Ca2+ blocker treatment of both MCF10A and NMuMG cells; this increase is not observed with 2APB treatment alone. Therefore, we believe that 2APB plays a synergistic role with TGF-β in Snail induction. We propose to investigate the gene networks that change following 2APB +TGF-β treatment.

2018-07-31 | GSE98596 | GEO

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