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HSP70.1 AND -70.3 ARE REQUIRED FOR LATE-PHASE PROTECTION INDUCED BY ISCHEMIC PRECONDITIONING OF MOUSE HEARTS
Citation:
Hampton, C. R., A. Shimamoto, C. L. Rothnie, J. GriscavageEnnis, A. Chong, D J. Dix, E. D. Verrier, AND T. H. Pohlman. HSP70.1 AND -70.3 ARE REQUIRED FOR LATE-PHASE PROTECTION INDUCED BY ISCHEMIC PRECONDITIONING OF MOUSE HEARTS. AMERICAN JOURNAL OF PHYSIOLOGY 285(2):866-874, (2003).
Description:
Heat-Shock Proteins 70.1 and 70.3 Are Required for Late-phase Protection
Induced by Ischemic Preconditioning of the Mouse Heart
Craig R. Hampton 1 , Akira Shimamoto 1 , Christine L. Rothnie 1 , Jeaneatte Griscavage-Ennis 1 ,
Albert Chong 1 , David J. Dix 2 , Edward D. Verrier 1 , and Timothy H. Pohlman 1
1 The Department of Surgery, The University of Washington, Box 359796, Seattle, WA 98104.
2 National Health and Environmental Effects Laboratory, Office of Research and Development,
U.S. Environmental Protection Agency, Research Triangle Park, North Carolina 27711.
Abstract
We investigated the role of inducible heat-shock proteins 70.1 (Hsp70.1) and 70.3
(Hsp70.3) in myocardial ischemic preconditioning (IP) in mice. Wild type (WT) mice and
Hsp70.1/3 null mice were subjected to IP and examined 24 hours later during the late phase of
protection. IP significantly increased steady-state levels of hsp70.1 and hsp70.3 mRNA, and
expression for inducible Hsp70 protein in WT myocardium. To assess protection against tissue
injury, mice were subjected to 30 minutes of regional ischemia and 3 hours of reperfusion (I/R).
In WT mice, IP reduced infarct size by 43% compared to sham IP-treated mice. In contrast, IP
did not reduce infarct size in Hsp70.1/3 null mice. Absence of inducible Hsp70.1 and 70.3 had
no effect, however, on classical, or early phase protection produced by IP, which significantly
reduced infarct size in Hsp70.1/3 null mice. We conclude that inducible Hsp70.1 and Hsp70.3
are required for late phase protection against infarction following IP in mice.