Li F, Wang X, Bunger P C, Gerdes A M
Department of Anatomy and Structural Biology, University of South Dakota, School of Medicine, Vermillion 57069, USA.
J Mol Cell Cardiol. 1997 Jun;29(6):1541-51. doi: 10.1006/jmcc.1997.0381.
Cardiac myocytes in rat hearts lose their ability to undergo cytokinesis between day 3 and day 4, resulting in the formation of binucleated myocytes. Failure in the formation of the actin-myosin contractile ring could cause cardiac myocytes to be defective in cytokinesis. Enzymatically isolated cardiac myocytes from 2- and 4-day-old rats were employed to investigate the organisation and distribution of actin, myomesin, and myosin by rhodamine phalloidin, anti-myomesin, and isoform-specific anti-myosin antibodies, respectively. Interestingly, the actin-myosin contractile ring was formed in mitotic myocytes from both 2- and 4-day-old animals. The changes in organisation and distribution of actin, myosin and myomesin in mitotic myocytes from 4-day-old rats were similar to those from 2-day-old rats, except that there were longitudinal actin filaments in the cytoplasm of mitotic myocytes from 4-day-old rats. In mitotic myocytes from both 2- and 4-day-old rats, actin disassembled in prometaphase, concentrated in the equator of the mitotic spindle in late anaphase, and formed a circumferential intensely staining band in early telophase. Cytoplasmic myosin was evenly distributed in the cytoplasm as small spots, and appeared to associate with the cell membrane from interphase to early anaphase. It became progressively more concentrated in association with the cortical membrane in the equator region in late anaphase, formed a ring-like structure in early telophase, and remained associated with adjacent membrane at the cleavage furrow until late telophase. Sarcomeric myosin and myomesin were only partially disassembled in mitotic myocytes from both 2- and 4-day-old animals. The present study showed that the actin-myosin contractile ring was actually formed during the binucleation process of cardiac myocytes. Molecules involved in the latter stages of cytokinesis may be responsible for incomplete cytokinesis during the binucleation process.
大鼠心脏中的心肌细胞在第3天到第4天之间失去进行胞质分裂的能力，导致双核心肌细胞的形成。肌动蛋白-肌球蛋白收缩环形成失败可能导致心肌细胞在胞质分裂中出现缺陷。分别用来自2日龄和4日龄大鼠的酶解分离心肌细胞，通过罗丹明鬼笔环肽、抗肌间线蛋白和同工型特异性抗肌球蛋白抗体来研究肌动蛋白、肌间线蛋白和肌球蛋白的组织和分布。有趣的是，来自2日龄和4日龄动物的有丝分裂心肌细胞中均形成了肌动蛋白-肌球蛋白收缩环。4日龄大鼠有丝分裂心肌细胞中肌动蛋白、肌球蛋白和肌间线蛋白的组织和分布变化与2日龄大鼠相似，只是4日龄大鼠有丝分裂心肌细胞的细胞质中有纵向肌动蛋白丝。在2日龄和4日龄大鼠的有丝分裂心肌细胞中，肌动蛋白在前中期解体，在后期晚期集中在有丝分裂纺锤体的赤道处，并在末期早期形成一个周向强染色带。细胞质肌球蛋白以小点状均匀分布在细胞质中，从间期到后期早期似乎与细胞膜相关联。在后期晚期，它在赤道区域与皮质膜相关联而逐渐变得更加集中，在末期早期形成环状结构，并在分裂沟处与相邻膜保持关联直至末期晚期。肌节肌球蛋白和肌间线蛋白在2日龄和4日龄动物的有丝分裂心肌细胞中仅部分解体。本研究表明，肌动蛋白-肌球蛋白收缩环实际上是在心肌细胞双核化过程中形成的。胞质分裂后期阶段涉及的分子可能是双核化过程中胞质分裂不完全的原因。
