Role of Calcium Signaling Pathway for Cardiac Cell Injury

在心肌中，钙离子在兴奋-收缩偶联中起着关键作用。在本研究中，我们研究了介导兴奋-收缩偶联的蛋白质在心肌损伤中的作用，并利用分子生物学的方法确定了磷蛋白与Ca-ATPase分子的相互作用部位。我们研究了磷蛋白和Ca-ATPase的基因调控，表明甲状腺激素是调节这些基因表达的关键因素。调节结合域位于心肌肌浆网钙释放通道中。缝隙连接的电生理研究表明，缝隙连接的活性受钙调蛋白的调节。我们纯化并测定了粘附素连接蛋白的一级结构。我们发现Rho是一种低分子量的G蛋白，它通过肌动球蛋白系统调节细胞的形态和运动。钙超载是心肌再灌注损伤的主要因素。这可能是由钙依赖的蛋白水解酶介导的。

In cardiac muscle, calcium plays a key role in excitation-contraction coupling. In this study, we investigated contribution of the proteins mediating excitation-contraction coupling for myocardial injury.We identified the interaction sites in phospholamban and the Ca ATPase molecule by using molecular biological methods. We investigated gene regulation of phospholamban and the Ca ATPase, indicating thyroid hormone is a key foactor for the regulation of those gene expression. Regulator binding domain was identified in the Ca release channel of the cardiac sarcoplasmic reticulum. Electrophysiological study on gap junction showed that the activity of gap junction is regulated by calmodulin. We purified and determined the primary structure of adherens junction proteins. We showed that a low molecular weight G-protein, rho regulates cell shape and mobility via actomyosin system.Calcium overload is a dominating factor for reperfusion injury of myocardium. This might mediated by Ca-dependent proteinase.