Activation of mitogen-activated protein kinases and p90 ribosomal S6 kinase in failing human hearts with dilated cardiomyopathy

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• 作者：Takeishi ; Yasuchika ; Huang ; Qunhua ; Abe ; Jun-ichi ; Che ; Wenyi ; Lee ; Jiing-Dwan ; Kawakatsu ; Hisaaki ; et. al.
• 关键词：Cardiomyopathy ; Heart failure ; Protein kinases ; Signal transduction
• 刊名：Cardiovascular Research
• 出版年：2002
• 期刊代码：48_00086363
• 类别：med
• 出版时间：January, 2002
• 卷：53
• 期：1
• 页码：131-137
• 文件大小：624 K

摘要

Objective: A new member of the MAP kinase family, big MAP kinase-1 (BMK1), has been recently identified to promote cell growth and attenuate apoptosis. P90 ribosomal S6 kinase (p90RSK), one of the potentially important substrates of extracellular signal regulated kinase (ERK), regulates gene expression in part via phosphorylation of CREB and the Na⁺/H⁺ exchanger. Recently, we have demonstrated that the activity of BMK1, Src (the upstream regulator of BMK1) and p90RSK was increased in hypertrophied myocardium induced by pressure-overload in the guinea pig. However, the abundance and activity of these kinases in human hearts are unknown. Methods: In addition to the three classical MAP kinases (ERK, p38 kinase, and c-Jun NH₂-terminal kinase (JNK)), we examined the protein expression and activity of Src, BMK1, and p90RSK in explanted hearts from patients with dilated cardiomyopathy (n