Undrovinas A I, Maltsev V A
Department of Cardiovascular Medicine, Henry Ford Heart and Vascular Institute, 2799 West Grand Boulevard, Detroit, MI, USA.
J Mol Cell Cardiol. 1998 Aug;30(8):1665-70. doi: 10.1006/jmcc.1998.0715.
The effects of cytochalasin D, a specific F-actin depolymerizing agent, on Ca2+ transients in rat ventricular cardiomyocytes were investigated. Cytochalasin D (20 microM) significantly slowed decay of Ca2+ transients (tau decay control cells=28.1+/-1.3, n=28tau decay=47.3+/-2.8 ms, n=20, P<0.001). The rising phase of Ca2+ transients was also significantly slower in cytochalasin D treated cells (tau rise=5.1+/-0.6 ms, n=17nu tau rise in control cells=3.6+/-0.2, n=21,P<0.01). Phalloidin (100 microM), an F-actin stabilizer, prevented cytochalasin D-induced alterations of Ca2+ transient kinetics. The cytochalasin D effect was not related to the l-type Ca2+ current since the current density and kinetics were not altered by the drug. We conclude that integrity of F-actin-based cytoskeleton is an important factor for sarcoplasmic reticulum function.
研究了细胞松弛素D（一种特异性F-肌动蛋白解聚剂）对大鼠心室心肌细胞Ca2+瞬变的影响。细胞松弛素D（20微摩尔）显著减慢了Ca2+瞬变的衰减（对照细胞的tau衰减=28.1±1.3，n=28；tau衰减=47.3±2.8毫秒，n=20，P<0.001）。在细胞松弛素D处理的细胞中，Ca2+瞬变的上升相也显著减慢（tau上升=5.1±0.6毫秒，n=17；对照细胞中的nu tau上升=3.6±0.2，n=21，P<0.01）。鬼笔环肽（100微摩尔），一种F-肌动蛋白稳定剂，可防止细胞松弛素D诱导的Ca2+瞬变动力学改变。细胞松弛素D的作用与L型Ca2+电流无关，因为该电流的密度和动力学未被该药物改变。我们得出结论，基于F-肌动蛋白的细胞骨架的完整性是肌浆网功能的一个重要因素。
