| First Author | Gao Y | Year | 2020 |
| Journal | Biochem Biophys Res Commun | Volume | 529 |
| Issue | 4 | Pages | 884-889 |
| PubMed ID | 32819594 | Mgi Jnum | J:302399 |
| Mgi Id | MGI:6508248 | Doi | 10.1016/j.bbrc.2020.05.220 |
| Citation | Gao Y, et al. (2020) Smooth muscle 22alpha deficiency impairs oxytocin-induced uterine contractility in mice at full-term pregnancy. Biochem Biophys Res Commun 529(4):884-889 |
| abstractText | Smooth muscle 22alpha (SM22alpha, namely Transgelin), as an actin-binding protein, regulates the contractility of vascular smooth muscle cells (VSMCs) by modulation of the stress fiber formation. However, little is known about the roles of SM22alpha in the regulation of uterine contraction during parturition. Here, we showed that contraction in response to oxytocin (OT) was significantly decreased in the uterine muscle strips from SM22alpha knockout (Sm22alpha-KO) mice, especially at full-term pregnancy, which may be resulted from impaired formation of stress fibers. Furthermore, serious mitochondrial damage such as the mitochondrial swelling, cristae disruption and even disappearance were observed in the myometrium of Sm22alpha-KO mice at full-term pregnancy, eventually resulting in the collapse of mitochondrial membrane potential and impairment in ATP synthesis. Our data indicate that SM22alpha is necessary to maintain uterine contractility at delivery in mice, and acts as a novel target for preventive or therapeutic manipulation of uterine atony during parturition. |
