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

GSE291516 Homo sapiens Expression profiling by high throughput sequencing 9 samples Submitted 2025/06/29 Platform GPL11154
Summary
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.
Published in
Ras-related protein 2 limits vascular smooth muscle cell phenotypic switching and abdominal aortic aneurysm development
Luo S, Chen J, Zhong K et al. · Nature communications 2025 · PMID 41145483 · doi:10.1038/s41467-025-64496-7
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Also filed as BioProject PRJNA1234073 and SRA study SRP569152. Searching any of these in the dataset finder brings you back here.

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