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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Modification of Ca2+-handling in cardiomyocytes by redox sensitive mechanisms in response to ouabain
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Modification of Ca2+-handling in cardiomyocytes by redox sensitive mechanisms in response to ouabain

机译：用氧化还原敏感机制响应对瓦巴恩的CA2 + -Handling的修饰

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摘要

We examined the role of redox-sensitive signal transduction mechanisms in modifying the changes in [Ca2+]i produced by ouabain upon incubating adult rat cardiomyocytes with antioxidants or inhibitors of different protein kinases and monitoring alterations in fura-2 fluorescence. Ouabain increased basal [Ca2+]i, augmented the KCl-induced increase in [Ca2+]i, and promoted oxyradical production in cardiomyocytes. These actions of ouabain were attenuated by an oxyradical scavenging mixture (superoxide dismutase plus catalase), and the antioxidants (N-acetyl-L-cysteine and N-(2-mercaptoproprionyl)glycine). An inhibitor of MAP kinase (PD98059) depressed the ouabain-induced increase in [Ca2+], whereas inhibitors of tyrosine kinase (tyrphostin and genistein) and PI3 kinase (Wortmannin and LV294002) enhanced the ouabain-induced increase in [Ca2+]i. Inhibitors of protein kinase C (calphostin and bisindolylmalaimide) augmented the ouabain-induced increase in [Ca2+]i, whereas stimulation of protein kinase C by a phorbol ester (phorbol 12-myristate 13-acetate) depressed the action of ouabain. These results suggest that ouabain-induced inhibition of Na +-K+ ATPase may alter the redox status of cardiomyocytes through the production of oxyradicals, and increase the activities of various protein kinases. Thus, these redox-sensitive signal transduction mechanisms involving different protein kinases may modify Ca2+-handling sites in cardiomyocytes and determine the magnitude of net increase in [Ca2+]i in response to ouabain.
机译：我们研究了氧化还原敏感信号转导机制在修饰奥巴班蛋白在孵育成年大鼠心肌细胞与不同蛋白激酶的抗氧化剂或抑制剂中的改变时改变奥巴班蛋白的变化以及监测呋喃-2荧光的改变。 Ouabain增加了基础[Ca2 +] I，增强了KCL诱导的[Ca2 +] I的增加，并在心肌细胞中促进过量的产量。 Ouabain的这些作用被一次性清除混合物（超氧化物歧化酶加酸酶）和抗氧化剂（N-乙酰基-1-半胱氨酸和N-（2-巯基丙烯基）甘氨酸）衰减。映射激酶（PD98059）抑制赋予Oubain诱导的[Ca2 +]的增加，而酪氨酸激酶（Tyrphostin和Genistein）和PI3激酶（Wortmannin和Lv294002）的抑制剂增强了oubain诱导的[Ca2 +] I的增加。蛋白激酶C的抑制剂（葫芦蛋白和双吲哚基甲基丙基酰亚胺）增强了Oubabain诱导的[Ca2 +] I的增加，而通过Phorbol酯刺激蛋白激酶C（Phorbol 12-醋酸酯13-醋酸酯）抑制瓦巴恩的作用。这些结果表明，威达诱导的Na + -K + ATP酶的抑制可以通过生产海洋生物的生产改变心肌细胞的氧化还原状态，并增加各种蛋白激酶的活性。因此，涉及不同蛋白激酶的这些氧化还原信号转导机制可以在心肌细胞中修饰Ca2 +手柄位点，并确定[Ca2 +] I的净增加的幅度响应于Ouabain。

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