Sarcoplasmic reticulum Ca(2+)ATPase and phospholamban mRNA and protein levels in end-stage heart failure due to ischemic or dilated cardiomyopathy
Sarcoplasmic reticulum Ca(2+)ATPase and phospholamban mRNA and protein levels in end-stage heart failure due to ischemic or dilated cardiomyopathy
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DOI：
10.1007/bf00207509
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发表时间：
1996-06-01
影响因子：
4.7
通讯作者：
Bohm, M
中科院分区：
文献类型：
--
作者：
Flesch, M;Schwinger, RHG;Bohm, M
细胞内Ca ~（2+）处理功能异常在心力衰竭的发病机制中起着重要作用。心肌衰竭时恢复静息低Ca ~（2+）水平的能力降低，其原因是肌浆网（SR）Ca（2+）ATP酶对Ca ~（2+）摄取的损害。目前尚不清楚Ca（2+）ATP酶功能、蛋白水平和mRNA稳态水平是否相互对应，以及心力衰竭的原因，即特发性扩张型或缺血性心肌病，是否产生不同的变化。本研究检测了8例非衰竭心脏、8例特发性扩张型心肌病（DCM）患者和6例缺血性心肌病（ICM）患者左心室肌SR Ca（2+）ATP酶活性以及SR Ca（2+）ATP酶、受磷蛋白和Gi α（2）的mRNA和蛋白水平。与非衰竭心肌相比，DCM患者衰竭心肌SR Ca（2+）ATP酶活性显著降低（36%，P
Abnormalities in intracellular Ca2+ handling play a crucial role in the pathogenesis of heart failure. The reduced capacity of failing human myocardium to restore low resting Ca2+ levels during diastole has been explained by the impairment of Ca2+ uptake into the sarcoplasmic reticulum (SR) via the SR Ca(2+)ATPase. It is unclear whether Ca(2+)ATPase function, protein levels, and mRNA steady-state levels correspond to one other, and whether the cause of heart failure, namely idiopathic dilated or ischemic cardiomyopathy, produces different changes. The present study examined SR Ca(2+)ATPase activity and both mRNA and protein levels of SR Ca(2+)ATPase, phospholamban, and Gi alpha(2) in left ventricular myocardium from eight nonfailing hearts, from eight hearts of patients with idiopathic dilated cardiomyopathy (DCM), and from six hearts from patients with ischemic cardiomyopathy (ICM). Compared to nonfailing myocardium, the activity of the SR Ca(2+)ATPase was significantly reduced in failing myocardium from patients with DCM (36%, P