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学科主题临床医学
Differential expression of 14-3-3 epsilon during physiological, pathological cardiac hypertrophy and chronic heart failure in mice
Qi, Jianyong; Xu, Ming; Lu, Zhizhen; Zhang, Youyi1
关键词14-3-3 Epsilon Protein Cardiac Hypertrophy Swimming Training Transverse Aortic Constriction
刊名GENE THERAPY AND MOLECULAR BIOLOGY
2009
13A页:71-81
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology ; Biotechnology & Applied Microbiology ; Medicine, Research & Experimental
资助者Foundation of National Key Basic Research and Development ; National Natural Science Foundation of China ; Foundation of National Key Basic Research and Development ; National Natural Science Foundation of China
研究领域[WOS]Biochemistry & Molecular Biology ; Biotechnology & Applied Microbiology ; Research & Experimental Medicine
关键词[WOS]SIGNAL-REGULATING KINASE-1 ; CREUTZFELDT-JAKOB-DISEASE ; 14-3-3 PROTEINS ; PRESSURE-OVERLOAD ; IN-VIVO ; CEREBROSPINAL-FLUID ; AMPHIPATHIC GROOVE ; P38 MAPK ; PHOSPHORYLATION ; ACTIVATION
英文摘要

Physiological cardiac hypertrophy associated with regular exercise is usually beneficial, in marked contrast to pathological hypertrophy associated with disease. 14-3-3 proteins play a critical antiapoptotic function in cardiomyocytes. Whether it or other genes activated in the athlete′s heart might have an impact on cardiac function and survival in a setting of heart failure is unknown. To examine whether different changes of 14-3-3 proteins expression in physiological cardiac hypertrophy, pathological cardiac hypertrophy and chronic heart failure (CHF), we constructed mouse models of physiological cardiac hypertrophy to swim training, pathological cardiac hypertrophy to transverse aortic constriction (TAC) for 4 weeks and chronic heart failure to TAC for 16 weeks. In response to swimming training and TAC, mice showed significant increases in left ventricular diastolic posterior wall thickness (LVPWd), heart weight and normalized heart weight to body weight ratio. However, in CHF mice, LVPWd decreased, end-diastolic volume (EDV) increased and marked cardiac fibrosis was formed. Thus, pressure overload induced decompensate heart failure and eccentric hypertrophy. Moreover, 14-3-3 epsilon protein expression of hearts was increased in response to swimming training but decreased in CHF mice. However, other isoforms (beta, zeta) of 14-3-3 proteins were no obvious changes in these three models. Therefore, our results suggest that the expressions of 14-3-3 epsilon are different in physiological and pathological hypertrophy, which may provide a potential gene strategy for the treatment of heart failure.

语种英语
所属项目编号2006CB503806 ; 30672466 ; 30821001
资助者Foundation of National Key Basic Research and Development ; National Natural Science Foundation of China ; Foundation of National Key Basic Research and Development ; National Natural Science Foundation of China
WOS记录号WOS:000268865200002
引用统计
被引频次:3[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/55977
专题北京大学第三临床医学院_心血管内科
作者单位1.Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing 100191, Peoples R China
2.Peking Univ, Inst Vasc Med, Hosp 3, Beijing 100191, Peoples R China
推荐引用方式
GB/T 7714
Qi, Jianyong,Xu, Ming,Lu, Zhizhen,et al. Differential expression of 14-3-3 epsilon during physiological, pathological cardiac hypertrophy and chronic heart failure in mice[J]. GENE THERAPY AND MOLECULAR BIOLOGY,2009,13A:71-81.
APA Qi, Jianyong,Xu, Ming,Lu, Zhizhen,&Zhang, Youyi.(2009).Differential expression of 14-3-3 epsilon during physiological, pathological cardiac hypertrophy and chronic heart failure in mice.GENE THERAPY AND MOLECULAR BIOLOGY,13A,71-81.
MLA Qi, Jianyong,et al."Differential expression of 14-3-3 epsilon during physiological, pathological cardiac hypertrophy and chronic heart failure in mice".GENE THERAPY AND MOLECULAR BIOLOGY 13A(2009):71-81.
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