Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA113643 | ENA |
REPOSITORIES: ENA
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Project description:Increased level of the hormone angiotensin II (AngII) contributes to the development of several cardiovascular issues, including atherosclerosis, vascular remodeling, and hypertension by altering gene expression. In our study, we use microarray analysis to investigate the effect of AngII on primary vascular smooth muscle cells derived from rat thoracic aorta. We have identified genes upregulated in response to AngII and are investigating their contribution to these cardiovascular conditions.
2024-11-28 | E-MTAB-14626 | biostudies-arrayexpress
Project description:Genetic Regulation of Vascular Smooth Muscle Cell Gene Expression and Atherosclerosis-relevant Phenotypes
| PRJNA573066 | ENA
Project description:The phenotypic switching of vascular smooth muscle cells (VSMCs) leads to neointimal hyperplasia, which is the underlying cause of vascular remodeling diseases such as atherosclerosis and hypertension. Novel hidden proteins encoded by circular RNAs (circRNAs) play crucial roles in disease progression. Our study identified a new protein derived from a circRNA in VSMCs and demonstrated its potential role in regulating vascular remodeling. We discovered a novel hidden protein, p-414aa, encoded by circSETD2(14,15), which can inhibit vascular remodeling. Both circSETD2(14,15) and p-414aa may serve as potential therapeutic targets for vascular remodeling diseases. In this study, we demonstrated that the new protein p-414aa encoded by circSETD2(14,15) inhibits VSMC proliferation and neointimal hyperplasia through the HuR/C-FOS axis. In summary, our data provide a molecular framework for the phenotypic switching of vascular smooth muscle cells.
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Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression.
2011-02-19 | GSE20463 | GEO
Project description:Increased level of angiotensin II (Ang II) plays a central role in the development of hypertensive vascular remodeling. Here, we identify the deubiquitinating enzyme JOSD2 as a protective factor and investigate its molecular mechanism in Ang II-induced vascular remodeling. Firstly, we found that JOSD2 was up-regulated in aortic smooth muscle cells but not endothelial cells of Ang II-challenged mouse vascular tissues. Whole-body knockout of JOSD2 significantly deteriorated Ang II-induced vascular remodeling in mice. Conversely, Ang II-induced vascular remodeling was reversed by VSMC-specific JOSD2 overexpression. In vitro, JOSD2 deficiency aggravated the fibrosis, proliferation, and migration induced by Ang II in vascular smooth muscle cells (VSMCs), while these changes were reversed by JOSD2 overexpression. RNA-seq analysis showed that the protective effects of JOSD2 in VSMCs were related to TGFβ-SMAD pathway. Furthermore, the LC-MS/MS analysis identified SMAD7, a negative regulator in TGFβ-SMAD pathway, as the substrate of JOSD2. JOSD2 specifically bound to the MH1 domain of SMAD7 to removed K48-linked Ub chains of SMAD7 at lysine 220 to sustain SMAD7 stability. Taken together, our finding reveals that JOSD2-SMAD7 axis is critical for relieving Ang II-induced vascular remodeling and JOSD2 maybe a novel and potential therapeutic target for hypertensive vascular remodeling.
2024-10-10 | PXD056674 | Pride
Project description:IL-1 plays an important role in atherosclerosis, and alters expression of a number of genes involved in atherosclerotic plaque development and progression. Smooth muscle cells play important roles in atherosclerotic plaque formation and stability, so this study was undertaken to determine the global effects of IL-1b on gene expression in smooth muscle cells in vitro. Cultured rat aortic smooth muscle cells were treated with IL-1b (2.5 ng/mL) or vehicle (0.1% BSA) for 24 hours prior to harvest.
2012-12-31 | E-GEOD-21403 | biostudies-arrayexpress
Project description:Vascular smooth muscle cells (VSMCs) are derived from distinct embryonic origins. Vessels originating from differing smooth muscle cell populations have distinct vascular and pathological properties of calcification, atherosclerosis, and structural defects such as aneurysm and coarctation. We hypothesized that domains within a vessel vary in phenotype based on embryonic origin. We used microarrays to detail the expression differences in vasculature of different embryonic origin. Mouse tissues were selected from different vascular compartments for RNA extraction and hybridization on Affymetrix microarrays. We sought to identify embryonic origin-specific expression profiles.
2014-08-26 | E-GEOD-50250 | biostudies-arrayexpress
Project description:Vascular smooth muscle cells (VSMCs) are derived from distinct embryonic origins. Vessels originating from differing smooth muscle cell populations have distinct vascular and pathological properties of calcification, atherosclerosis, and structural defects such as aneurysm and coarctation. We hypothesized that domains within a vessel vary in phenotype based on embryonic origin. We used microarrays to detail the expression differences in vasculature of different embryonic origin. Mouse tissues were selected from different vascular compartments for RNA extraction and hybridization on Affymetrix microarrays. We sought to identify embryonic origin-specific expression profiles.
2014-08-26 | E-GEOD-50251 | biostudies-arrayexpress
Project description:Gene methylation profiling of immortalized human mesenchymal stem cells comparing HPV E6/E7-transfected MSCs cells with human telomerase reverse transcriptase (hTERT)- and HPV E6/E7-transfected MSCs. hTERT may increase gene methylation in MSCs. Goal was to determine the effects of different transfected genes on global gene methylation in MSCs.
2011-08-25 | GSE23936 | GEO
Project description:Enhancer-associated LncRNA-ITGA2 promotes vascular smooth muscle remodeling by mediating ITGA2 promoter-enhancer interactions
| PRJNA1225434 | ENA