[総説］血管平滑筋Ca2^<2+>チャネルの調節機構 : アクチンフィラメントの意義

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概要

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• Changes in the cytoskeletal network alter the mechanical properties of cells that are essential for functions such as locomotion and cytokinesis. The transmembrane receptors and intracellular signals have been extensively studied on cytoskeletal changes in response to extracellular stimuli. After the procedure of percutaneous transluminal coronary angioplasty (PTCA) and highfrequency rotational atherectomy (PTCR) for stenosis of blood vessels, restenosis may be observed. The restenosis were generated under the proliferation and migration of vascular smooth muscle (VSM) cells. In addition, until recently it has been expected that the physiological regulation of VSM cells was dependent on L-type Ca^<2+> (Ca_1) channel activity and structure of the cytoskeleton. To clarify the interactions between the structure of the cytoskeleton and activity of Ca_1 channel in VSM cell, we used electrophysiological and morphological experiments concomitantly. We investigated the effect of disruption of the actin filaments and the microtubules on Ca_1 channel activity (Ca^<2+> current) of cultured VSM cells (A7r5 cell line) using whole cell voltage clamp. The results of immunostaining using anti-$ \alpha $-actin and anti-$ \alpha $-tubulin antibodies showed that colchicines disrupted both actin filaments and microtubules, while cytochalasin D and nocodazole disrupted only actin filaments, and microtubules respectively. Ca^<2+> current was greatly reduced in cells that were exposed to colchicines or cytochalasin D but not to nocodazole. When the actin filaments were stabilized by phalloidine, the inhibition of Ca^<2+> current was not observed. Actin filaments disruption of VSM cells inhibits Ca_1 channel activity, whereas the microtubules disruption gave no effect on the activity. These results suggested that the maintenance of physiological function in VSM cells involve the functional-structural relationship between the Ltype Ca^<2+> channel and cytoskeleton. The development of restenosis is dependent on the pathophysiological proliferation and then migration of the VSM cells could be prevented by control of L-type Ca^<2+> channel activity and stabilization of the cytoskeleton in VSM cells.

• 琉球医学会,Ryukyu Medical Associationの論文

琉球医学会,Ryukyu Medical Association | 論文

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