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Enhanced myocardial cathepsin B expression in patients with dilated cardiomyopathy
Author(s) -
Ge Junbo,
Zhao Gang,
Chen Ruizhen,
Li Shuangjie,
Wang Shijun,
Zhang Xingang,
Zhuang Yamin,
Du Jiuzhong,
Yu Xiaohua,
Li Gaoping,
Yang Yingzhen
Publication year - 2006
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1016/j.ejheart.2005.09.004
Subject(s) - cathepsin b , heart failure , medicine , dilated cardiomyopathy , cathepsin , cathepsin s , cathepsin d , tunel assay , immunohistochemistry , cardiology , endocrinology , biology , enzyme , biochemistry
Objective Cathepsin B is a prominent lysosomal protease and is involved in apoptosis as well as degradation of myofibrillar proteins in myocardial infarction. The aim of this study was to investigate myocardial cathepsin B expression in failing and non‐failing human hearts. Methods: Tissue samples were taken from transplanted left ventricles from 20 patients with dilated cardiomyopathy and 5 non‐failing donor hearts that could not be transplanted for technical reasons. Myocardial cathepsin B expression was determined by immunohistochemistry, the reverse transcription–polymerase chain reaction (RT–PCR) and Western blotting. Apoptosis was assessed by TUNEL staining. Results: Positive cathepsin B staining was found in failing and non‐failing hearts. The expression of cathepsin B at mRNA and protein levels was significantly higher in failing hearts compared with non‐failing hearts. Correlation analysis revealed that cathepsin B at mRNA and protein levels negatively correlated with EF ( r =0.66, p =0.002 and r =0.492, p =0.028, respectively) in patients with heart failure. The apoptotic index was 0.015±0.006 in failing hearts and 0.002±0.001 in non‐failing hearts ( p <0.01). Conclusion: Increased myocardial expression of cathepsin B was found in patients with heart failure suggesting that cathepsin B might play a role in the genesis and development of heart failure.