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首页> 外文期刊>Cellular Physiology and Biochemistry >Vascular smooth muscle contraction evoked by cell volume modulation: Role of the cytoskeleton network
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Vascular smooth muscle contraction evoked by cell volume modulation: Role of the cytoskeleton network

机译：细胞体积调节引起的血管平滑肌收缩：细胞骨架网络的作用

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Previously, we reported that hyposmotic swelling evoked transient vascular smooth muscle cell ( SMC) contraction that was completely abolished by L-type Ca2+ channel blockers. In contrast, sustained contraction revealed in hyper- and isoosmotically-shrunken SMCs was insensitive to L-type channel blockers and was diminished in Ca2+- free medium by only 30-50%. Several research groups reported cell volume-dependent cytoskeleton network rearrangements. This study examines the role of cytoskeleton proteins in cell volume-dependent contraction of endothelium-denuded vascular smooth muscle rings (VSMR) from the rat thoracic aorta. Hyperosmotic shrinkage and hyposmotic swelling were triggered by modulation of medium osmolality; isosmotic shrinkage was induced by VSMR transfer from hypo- to isosmotic medium. The relative content of globular (G) and fibrillar (F) actin was estimated by fluorescence microscopy. Hyperosmotic shrinkage and hyposmotic swelling led to elevation of the F-actin/G-actin ratio by 2.5- and 1.8- fold respectively. Contraction of shrunken and swollen VSMR was insensitive to modulators of microtubules such as vinblastine, colchicine and docetaxel. Microfilament disassembly by cytochalasin B resulted in dramatic attenuation of the maximal amplitude of contraction of hyperosmotically-shrunken and hyposmotically-swollen VSMR, and almost completely abolished the contraction triggered by isosmotic shrinkage. These data suggest that both L-type Ca2+ channel-mediated contraction of swollen vascular SMC and Ca2+ -insensitive contractions of shrunken cells are triggered by reorganization of the microfilament network caused by elevation of the F-actin/G-actin ratio. Copyright (c) 2008 S. Karger AG, Basel.
机译：以前，我们报道过低渗性肿胀引起短暂的血管平滑肌细胞（SMC）收缩，而L型Ca2 +通道阻滞剂完全消除了该收缩。相反，高收缩和等渗收缩的SMC中显示的持续收缩对L型通道阻滞剂不敏感，在无Ca2 +的培养基中仅减少30-50％。几个研究小组报告了细胞体积依赖性细胞骨架网络重排。这项研究检查了细胞骨架蛋白在大鼠胸主动脉内皮剥除的血管平滑肌环（VSMR）的细胞体积依赖性收缩中的作用。高渗收缩和低渗肿胀是由中等渗透压调节引起的。等渗收缩是由VSMR从低渗介质转移到等渗介质引起的。球状（G）和原纤维（F）肌动蛋白的相对含量通过荧光显微镜评估。高渗性收缩和低渗性溶胀分别导致F-肌动蛋白/ G-肌动蛋白比提高2.5倍和1.8倍。收缩和肿胀的VSMR的收缩对微管的调节剂（如长春碱，秋水仙碱和多西他赛）不敏感。细胞松弛素B分解微丝导致高渗透性收缩和低渗透性膨胀VSMR的最大收缩幅度显着减弱，并且几乎完全消除了等渗收缩引起的收缩。这些数据表明，由F-肌动蛋白/ G-肌动蛋白比例升高引起的微丝网络重组触发了L型Ca2 +通道介导的溶胀性血管SMC收缩和Ca2 +不敏感的收缩细胞收缩。版权所有（c）2008 S. Karger AG，巴塞尔。

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