| First Author | Feng HZ | Year | 2019 |
| Journal | J Mol Cell Cardiol | Volume | 129 |
| Pages | 49-57 | PubMed ID | 30707993 |
| Mgi Jnum | J:276077 | Mgi Id | MGI:6305027 |
| Doi | 10.1016/j.yjmcc.2019.01.026 | Citation | Feng HZ, et al. (2019) Double deletion of calponin 1 and calponin 2 in mice decreases systemic blood pressure with blunted length-tension response of aortic smooth muscle. J Mol Cell Cardiol 129:49-57 |
| abstractText | Calponin is a family of actin filament-associated regulatory proteins. Among its three isoforms, calponin 1 is smooth muscle specific and calponin 2 is expressed in smooth muscle and certain non-muscle cells. Previous studies showed that calponin 1 knockout mice had detectable changes in the contractility of urogenital smooth muscle whereas other smooth muscles were less affected. To investigate the possibility that calponins 1 and 2 have overlapping functions in smooth muscle, we examined the effect of double knockout of calponin 1 and calponin 2 genes (Cnn1 and Cnn2) on smooth muscle functions. The results showed for the first time that calponin 1 and calponin 2 double knockout in mice does not cause lethality. The double knockout mice showed decreased systemic blood pressure, decreased force development and blunted length tension response in endothelial-removed aortic rings. A compensatory increase of calponin 1 was found in smooth muscle of Cnn2(-/-) mice but not vice versa. Cnn1(-/-) and Cnn2(-/-) double knockout aortic smooth muscle exhibits faster relaxation than that of wild type control. Double deletion or co-suppression of calponin 1 and calponin 2 in vascular smooth muscle to blunt myogenic response may present a novel approach to develop new treatment for hypertension. |
