AGONIST-INDUCED REDISTRIBUTION OF CALPONIN IN CONTRACTILE VASCULAR SMOOTH-MUSCLE CELLS
AGONIST-INDUCED REDISTRIBUTION OF CALPONIN IN CONTRACTILE VASCULAR SMOOTH-MUSCLE CELLS
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DOI：
10.1152/ajpcell.1994.267.5.c1262
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发表时间：
1994-11-01
影响因子：
5.5
通讯作者：
MORGAN, KG
中科院分区：
文献类型：
--
作者：
PARKER, CA;TAKAHASHI, K;MORGAN, KG
Calponin是一种细丝相关蛋白，被认为在平滑肌收缩中起辅助调节作用。我们使用免疫荧光和数字成像显微镜来确定新鲜从雪貂门静脉分离的单个细胞中钙蛋白的细胞分布。在静息细胞中，钙粘蛋白分布在整个胞浆中，与丝状结构有关，不在细胞的核区。表面皮质相关的钙蛋白与胞浆相关的钙蛋白(R)的比值为0.639+/-0.021。在细胞去极化时。在含96 mM K+的生理盐水溶液中，钙蛋白的分布与静息细胞无明显变化(R=0.678+/-0.025，P=0.369)。用激动剂(10 mU苯肾上腺素)刺激后，细胞内钙蛋白的分布由胞浆为主转变为以表层皮质为主(R=1.24+/-0.085，P<0.001)。这种激动剂诱导的钙蛋白重新分布部分地被PKC抑制剂Calphostin抑制，在时间上与PKC转位重叠，并先于这些细胞的收缩。这些结果表明，Calponin的生理功能可能是通过依赖于PKC的途径来介导激动剂激活的收缩。
Calponin is a thin filament-associated protein that has been implicated in playing an auxiliary regulatory role in smooth muscle contraction. We have used immunofluorescence and digital imaging microscopy to determine the cellular distribution of calponin in single cells freshly isolated from the ferret portal vein. In resting cells calponin is distributed throughout the cytosol, associated with filamentous structures, and is excluded from the nuclear area of the cell. The ratio of surface cortex-associated calponin to cytosol-associated calponin (R) was found to be 0.639 +/- 0.021. Upon depolarization of the cell. with physiological saline solution containing 96 mM K+, the distribution of calponin did not change from that of a resting cell (R = 0.678 +/- 0.025, P = 0.369). Upon stimulation with an agonist (10 mu M phenylephrine) that is known to activate protein kinase C (PKC) in these cells, the cellular distribution of calponin changed from primarily cytosolic to primarily surface cortex associated (R = 1.24 +/- 0.085, P < 0.001). This agonist-induced redistribution of calponin was partially inhibited by the PKC inhibitor calphostin, overlapped in time with PKC translocation, and preceded contraction of these cells. These results suggest that the physiological function of calponin may be to mediate agonist-activated contraction via a PKC-dependent pathway.