Smooth muscle 22α deficiency impairs oxytocin-induced uterine contractility in mice at full-term pregnancy
Smooth muscle 22α deficiency impairs oxytocin-induced uterine contractility in mice at full-term pregnancy
复制标题
平滑肌 22α 缺乏会损害足月妊娠小鼠催产素诱导的子宫收缩力
DOI：
10.1016/j.bbrc.2020.05.220
复制
发表时间：
2020-09-03
影响因子：
3.1
通讯作者：
Han, Mei
中科院分区：
文献类型：
--
作者：
Gao, Yakun;Liu, Guixia;Han, Mei
Smooth muscle 22 alpha (SM22 alpha, 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 SM22 alpha 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 SM22 alpha knockout (Sm22 alpha-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 Sm22 alpha-KO mice at full-term pregnancy, eventually resulting in the collapse of mitochondrial membrane potential and impairment in ATP synthesis. Our data indicate that SM22 alpha 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. (C) 2020 Elsevier Inc. All rights reserved.
