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Ras-related protein 2 limits vascular smooth muscle cell phenotypic switching and abdominal aortic aneurysm development

ABSTRACT: Ras-related protein 2 limits vascular smooth muscle cell phenotypic switching and abdominal aortic aneurysm development

PROVIDER: PRJNA1234073 | ENA |

REPOSITORIES: ENA

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Project description:Abdominal aortic aneurysm (AAA) and the attendant catastrophic event of rupture remain a leading cause of death. During AAA, VSMCs lost contractile-related phenotype, with reduced levels of actin alpha 2, smooth muscle (ACTA2), transgelin (TAGLN) and calponin 1 (CNN1)) , and obtain ability to secrete matrix metalloproteinases to degrade the extracellular matrix and weaken the arterial wall, which potentiate the rupture of the aneurysm. Angiotensin 2 (Ang II) can induce phenotype transition of VSMCs，while the underlying mechanism remains elusive. Here we found Ang II treatment could reduce expression of R-Ras2, thus reducing the phosphorylation and nuclear translocation of TFII-I, as a result, the gene expression of ACTA2, TAGLN and CNN1 were inhibited and VSMCs lost the contractile phenotype.

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Project description:Abdominal aortic aneurysm (AAA) is a permanent segmental dilatation of the abdominal aorta, contributing to a high mortality once rupture. We performed RNA-sequencing analysis of abdominal aorta tissues from 14 participants, including seven patients with AAA and seven control individuals.

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scRNA-seq of Abdominal aortic aneurysm tissues in Gsdme-KO mice

Project description:The aim of this study was to explore the transciptome of the diverse vascular smooth muscle cells subsets from abdominal aortic aneurysm tissues in Gsdme deletion mice.The model was established by exposing the infrarenal aorta to PPE (porcine pancreatic elastase) under pressure to induce aneurysmal degeneration for 4 weeks.we compared the characteristics of SMC subpopulation beteew the WT and KO groupsto reveal the effect of GSDME in the progression of Abdomanl Aortic Aneurysm.

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Differential gene expression in human abdominal aortic aneurysm and atherosclerosis

Project description:The aim of this study was to assess the relative gene expression in human AAA and AOD. Genome-wide expression analysis of abdominal aortic aneurysm (AAA) and aortic occlusive disease (AOD) specimens obtained from 20 patients with small AAA (mean maximum aortic diameter=54.3±2.3 mm), 29 patients with large AAA (mean maximum aortic diameter=68.4±14.3 mm), and 9 AOD patients (mean maximum aortic diameter=19.6±2.6 mm). Relative aortic gene expression was compared with that of 10 control aortic specimen of organ donors.

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Aorta proteomic analysis thoracic-abdominal

Project description:Aortic aneurysms is increasing as the human population ages. Pathological oxidative stress is implicated in development of aortic aneurysms. We pursued a chemogenetic approach to create an animal model of aortic aneurysm formation using a transgenic mouse line DAAO-TGTie2 that expresses yeast D-amino acid oxidase (DAAO) under control of the endothelial Tie2 promoter. In DAAO-TGTie2 mice, DAAO generates the reactive oxygen species hydrogen peroxide (H2O2) in endothelial cells only when provided with D-amino acids. When DAAO-TGTie2 mice are chronically fed D-alanine, the animals become hypertensive and develop abdominal but not thoracic aortic aneurysms. Generation of H2O2 in the endothelium leads to oxidative stress throughout the vascular wall. Proteomic analyses indicate that the oxidant-modulated protein kinase JNK1 is dephosphorylated by the phophoprotein phosphatase DUSP3 in abdominal but not thoracic aorta, causing activation of KLF4-dependent transcriptional pathways that trigger phenotypic switching and aneurysm formation. Pharmacological DUSP3 inhibition completely blocks aneurysm formation caused by chemogenetic oxidative stress. These studies establish that regional differences in oxidant-modulated signaling pathways lead to differential disease progression in discrete vascular beds, and identify DUSP3 as a potential pharmacological target for the treatment of aortic aneurysms.

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