HSP70.1 and -70.3 are required for late-phase protection induced by ischemic preconditioning of mouse hearts
| Autor: | Jeaneatte Griscavage-Ennis, Albert J. Chong, Craig R. Hampton, Edward D. Verrier, Akira Shimamoto, David J. Dix, Timothy H. Pohlman, Christine L. Rothnie |
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| Rok vydání: | 2003 |
| Předmět: |
Pathology
medicine.medical_specialty Cytoplasm Physiology Ratón Ischemia Myocardial Infarction Protozoan Proteins Gene Expression Myocardial Reperfusion Injury Pharmacology Mice Physiology (medical) Heat shock protein medicine Animals HSP70 Heat-Shock Proteins RNA Messenger Mice Knockout business.industry medicine.disease Hsp70 Mice Inbred C57BL Circulatory system Knockout mouse Ischemic Preconditioning Myocardial Ischemic preconditioning Cardiology and Cardiovascular Medicine business Reperfusion injury |
| Zdroj: | American journal of physiology. Heart and circulatory physiology. 285(2) |
| ISSN: | 0363-6135 |
| Popis: | We investigated the role of inducible heat shock proteins 70.1 and 70.3 (HSP70.1 and HSP70.3, respectively) in myocardial ischemic preconditioning (IP) in mice. Wild-type (WT) mice and HSP70.1- and HSP70.3-null [HSP70.1/3(–/–)] mice were subjected to IP and examined 24 h later during the late phase of protection. IP significantly increased steady-state levels of HSP70.1 and HSP70.3 mRNA and expression of inducible HSP70 protein in WT myocardium. To assess protection against tissue injury, mice were subjected to 30 min of regional ischemia and 3 h of reperfusion. In WT mice, IP reduced infarct size by 43% compared with sham IP-treated mice. In contrast, IP did not reduce infarct size in HSP70.1/3(–/–) mice. Absence of inducible HSP70.1 and HSP70.3 had no effect, however, on classical or early-phase protection produced by IP, which significantly reduced infarct size in HSP70.1/3(–/–) mice. We conclude that inducible HSP70.1 and HSP70.3 are required for late-phase protection against infarction following IP in mice. |
| Databáze: | OpenAIRE |
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