Simpson D G, Sharp W W, Borg T K, Price R L, Samarel A M, Terracio L
Department of Developmental Biology and Anatomy, University of South Carolina School of Medicine, Columbia 29208, USA.
Ann N Y Acad Sci. 1995 Mar 27;752:131-40. doi: 10.1111/j.1749-6632.1995.tb17416.x.
The excitation-contraction coupling cycle (ECC) consists of a complex cascade of electrochemical and mechanical events; however, the relative contributions of these different processes in the regulation of cardiac myofibrillar structure are not well understood. There is extensive evidence to suggest that the mechanical aspects of the ECC play a crucial role in controlling the availability of contractile proteins for myofibrillar assembly. To examine if these physical forces might also serve to stabilize the structure of preexisting myofibrils, beating and nonbeating cultures of neonatal cardiac myocytes (NCM) were subjected to a 5% static stretch. Contractile arrest was achieved by treating NCM with 12 microM nifedipine, which resulted in immediate and sustained contractile arrest and initiated the evolution of marked myofibrillar abnormalities within 24 hours. As judged by scanning confocal and transmission electron microscopic examination, an external load appears to partially stabilize myofibrillar structure in nonbeating NCM. These results suggest that the maintenance of myofibrillar structure may be highly dependent upon the mechanical aspects of ECC.
兴奋 - 收缩偶联循环(ECC)由一系列复杂的电化学和机械事件组成;然而,这些不同过程在心肌肌原纤维结构调节中的相对作用尚未得到充分理解。有大量证据表明,ECC的机械方面在控制收缩蛋白用于肌原纤维组装的可用性方面起着关键作用。为了研究这些物理力是否也有助于稳定已存在的肌原纤维结构,对新生心肌细胞(NCM)的搏动和非搏动培养物施加5%的静态拉伸。通过用12微摩尔硝苯地平处理NCM实现收缩停止,这导致立即且持续的收缩停止,并在24小时内引发明显的肌原纤维异常演变。通过扫描共聚焦和透射电子显微镜检查判断,外部负荷似乎部分稳定了非搏动NCM中的肌原纤维结构。这些结果表明,肌原纤维结构的维持可能高度依赖于ECC的机械方面。