期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：1999
卷号：96
期号：22
页码：12798-12803
DOI：10.1073/pnas.96.22.12798
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Brief periods of cardiac ischemia trigger protection from subsequent prolonged ischemia (preconditioning). {varepsilon} Protein kinase C ({varepsilon}PKC) has been suggested to mediate preconditioning. Here, we describe an {varepsilon}PKC-selective agonist octapeptide, {psi}{varepsilon} receptor for activated C-kinase ({psi}{varepsilon}RACK), derived from an {varepsilon}PKC sequence homologous to its anchoring protein, {varepsilon}RACK. Introduction of {psi}{varepsilon}RACK into isolated cardiomyocytes, or its postnatal expression as a transgene in mouse hearts, increased {varepsilon}PKC translocation and caused cardio-protection from ischemia without any deleterious effects. Our data demonstrate that {varepsilon}PKC activation is required for protection from ischemic insult and suggest that small molecules that mimic this {varepsilon}PKC agonist octapeptide provide a powerful therapeutic approach to protect hearts at risk for ischemia.
