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• W2145301841 abstract "We previously showed that ablation of caveolin-1 (Cav-1) gene expression in mice promotes neointimal hyperplasia in vivo, a phenomenon normally characterized by smooth muscle cell (SMC) migration and proliferation. Whether these defects are cell autonomous, i.e., due to loss of Cav-1 within SMCs or loss of Cav-1 expression in other adjacent cell types in vivo, remains unknown. Cav-1 has been shown to associate with receptors for many vasoactive factors on the SMC surface. Therefore, Cav-1 might be an important regulator of SMC proliferation, migration, and signal transduction. To mechanistically dissect the role of Cav-1 in SMC signaling, we isolated SMCs from the aortas (AoSMCs) of Cav-1-deficient (Cav-1(-/-)) mice and characterized these cells with respect to their proliferation, migration, and Ca(2+) response to an important vasoactive factor, endothelin-1 (ET-1). 5-Bromo-2'-deoxyuridine incorporation and a wound-healing assay showed an increase in proliferation and migration rates in Cav-1(-/-) compared with wild-type (Cav-1(+/+)) AoSMCs. Cav-1(-/-) AoSMCs demonstrated upregulation of phosphorylated ERK1/2, cyclin D1, and proliferating cell nuclear antigen and reduced expression of the cyclin-dependent kinase inhibitor p27(Kip1). The Ca(2+) response was examined in the presence of ET-1 and assessed by confocal microscopy with the Ca(2+)-sensitive fluorescent probe fluo 3. When treated with ET-1, Cav-1(-/-) AoSMCs exhibited a faster and larger increase in free intracellular Ca(2+) than Cav-1(+/+) cells. The ET-1-induced response in Cav-1(-/-) cells was mediated by the ET(B) receptor, as shown using the ET(B) receptor antagonist BQ-788 and the ET(A) receptor antagonist BQ-123. In Cav-1(-/-) cells, ET(A) receptor expression was reduced and ET(B) receptor expression was upregulated. Therefore, Cav-1 ablation increased the ET-1-induced Ca(2+) response in SMCs by altering the type and expression level of the ET receptor (i.e., receptor isoform switching). These data suggest a novel regulatory role for Cav-1 in SMCs with respect to their proliferation, migration, and Ca(2+)-mediated signaling." @default.
• W2145301841 created "2016-06-24" @default.
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• W2145301841 date "2006-06-01" @default.
• W2145301841 modified "2023-09-30" @default.
• W2145301841 title "Caveolin-1-deficient aortic smooth muscle cells show cell autonomous abnormalities in proliferation, migration, and endothelin-based signal transduction" @default.
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• W2145301841 doi "https://doi.org/10.1152/ajpheart.01161.2005" @default.
• W2145301841 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16415072" @default.
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