| First Author | Islam S | Year | 2020 |
| Journal | J Physiol Sci | Volume | 70 |
| Issue | 1 | Pages | 18 |
| PubMed ID | 32192434 | Mgi Jnum | J:302517 |
| Mgi Id | MGI:6508194 | Doi | 10.1186/s12576-020-00745-2 |
| Citation | Islam S, et al. (2020) Class II phosphatidylinositol 3-kinase alpha and beta isoforms are required for vascular smooth muscle Rho activation, contraction and blood pressure regulation in mice. J Physiol Sci 70(1):18 |
| abstractText | Class II phosphatidylinositol 3-kinases (PI3K), PI3K-C2alpha and PI3K-C2beta, are involved in cellular processes including endocytosis, cilia formation and autophagy. However, the role of PI3K-C2alpha and PI3K-C2beta at the organismal level is not well understood. We found that double knockout (KO) mice with both smooth muscle-specific KO of PI3K-C2alpha and global PI3K-C2beta KO, but not single KO mice of either PI3K-C2alpha or PI3K-C2beta, exhibited reductions in arterial blood pressure and substantial attenuation of contractile responses of isolated aortic rings. In wild-type vascular smooth muscle cells, double knockdown of PI3K-C2alpha and PI3K-C2beta but not single knockdown of either PI3K markedly inhibited contraction with reduced phosphorylation of 20-kDa myosin light chain and MYPT1 and Rho activation, but without inhibition of the intracellular Ca(2+) mobilization. These data indicate that PI3K-C2alpha and PI3K-C2beta play the redundant but essential role for vascular smooth muscle contraction and blood pressure regulation mainly through their involvement in Rho activation. |
