| First Author | Lv P | Year | 2016 |
| Journal | Am J Physiol Cell Physiol | Volume | 311 |
| Issue | 5 | Pages | C758-C767 |
| PubMed ID | 27629412 | Mgi Jnum | J:237265 |
| Mgi Id | MGI:5811923 | Doi | 10.1152/ajpcell.00033.2016 |
| Citation | Lv P, et al. (2016) SM22alpha inhibits lamellipodium formation and migration via Ras-Arp2/3 signaling in synthetic VSMCs. Am J Physiol Cell Physiol 311(5):C758-C767 |
| abstractText | We previously demonstrated that smooth muscle (SM) 22alpha promotes the migration activity in contractile vascular smooth muscle cells (VSMCs). Based on the varied functions exhibited by SM22alpha in different VSMC phenotypes, we investigated the effect of SM22alpha on VSMC migration under pathological conditions. The results demonstrated that SM22alpha overexpression in synthetic VSMCs inhibited platelet-derived growth factor (PDGF)-BB-induced cell lamellipodium formation and migration, which was different from its action in contractile cells. The results indicated two distinct mechanisms underlying inhibition of lamellipodium formation by SM22alpha, increased actin dynamic stability and decreased Ras activity via interference with interactions between Ras and guanine nucleotide exchange factor. The former inhibited actin cytoskeleton rearrangement in the cell cortex, while the latter significantly disrupted actin nucleation activation of the Arp2/3 complex. Baicalin, a herb-derived flavonoid compound, inhibited VSMC migration via upregulation of SM22alpha expression in vitro and in vivo. These data suggest that SM22alpha regulates lamellipodium formation and cell migration in a phenotype-dependent manner in VSMCs, which may be a new therapeutic target for vascular lesion formation. |
