NDLI: Heart-targeted overexpression of caspase3 in mice increases infarct size and depresses cardiac function.

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Heart-targeted overexpression of caspase3 in mice increases infarct size and depresses cardiac function.

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Heart-targeted overexpression of caspase3 in mice increases infarct size and depresses cardiac function.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Frati, G. Napoli, C. Russo, M. A. Roncarati, R. Drusco, A. Lefer, D. J. Stassi, G. Croce, C. M. Ross, J. Condorelli, G. Jones, S. P. Pisani, A. Todaro, M. Gu, Y. Trocha, S.
Description	Author Affiliation: Condorelli G ( Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107-5541, USA. gianluigi.condorelli@mail.tju.edu);
Abstract	Up-regulation of proapoptotic genes has been reported in heart failure and myocardial infarction. To determine whether caspase genes can affect cardiac function, a transgenic mouse was generated. Cardiac tissue-specific overexpression of the proapoptotic gene Caspase3 was induced by using the rat promoter of alpha-myosin heavy chain, a model that may represent a unique tool for investigating new molecules and antiapoptotic therapeutic strategies. Cardiac-specific Caspase3 expression induced transient depression of cardiac function and abnormal nuclear and myofibrillar ultrastructural damage. When subjected to myocardial ischemia-reperfusion injury, Caspase3 transgenic mice showed increased infarct size and a pronounced susceptibility to die. In this report, we document an unexpected property of the proapoptotic gene caspase3 on cardiac contractility. Despite inducing ultrastructural damage, Caspase3 does not trigger a full apoptotic response in the cardiomyocyte. We also implicate Caspase3 in determining myocardial infarct size after ischemia-reperfusion injury, because its cardiomyocyte-specific overexpression increases infarct size.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	17
Volume Number	98
Language	English
Publisher	National Academy of Sciences
Publisher Date	2001-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Caspases Physiology Myocardial Infarction Enzymology Myocardial Reperfusion Injury Myocardium Ventricular Dysfunction, Left Animals Apoptosis Genetics Caspase 3 DNA Fragmentation DNA, Complementary Echocardiography Gene Expression Regulation Genetic Predisposition To Disease Mice Mice, Transgenic Pathology Myocardial Ischemia Organ Specificity Phenotype Recombinant Fusion Proteins Etiology Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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