title: Myocardial heat shock proteins during the development of heart failure.
abstract: When cardiomyocytes are exposed to stresses, production of heat shock proteins (HSPs) in the cells is enhanced. Such increase in cellular HSP production is considered to bring about tolerance against stress-induced cell damage. The exact role of the cellular HSPs remains unclear. In the present study, HSPs in the viable left ventricular myocardium were determined during the development of heart failure following coronary artery ligation (CAL). The rats after CAL showed symptoms of chronic heart failure (CHF) at the 8th week, but not at the 1st and 2nd weeks. Myocardial HSP27, which may bind to cytoskeletal protein, at the 1st, 2nd, and 8th weeks after CAL was approximately 180, 160, and 125% of the control, respectively. Myocardial HSP60, one of mitochondrial proteins, at the 8th week increased to 140% of the control, whereas those at the 1st and 2nd weeks did not change. Myocardial HSP72, an inducible form of HSP70 family, at the 1st week after CAL increased to 180% of the control, whereas that at the 2nd or 8th week was similar to control. Myocardial heat shock constitutive protein 73 (HSC73), a constitutively expressed form of HSP70 family, and HSP90, which may bind to steroid hormone receptor and actin fiber, of CAL rats did not alter throughout the experiment. These findings show that diverse changes in the production of myocardial HSPs occur during the development of heart failure. Only the increase in myocardial HSP60 production was associated with the development of CHF.
authors.affiliation: Department of Pharmacology, Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi, Hachioji, Tokyo, 192-0392, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Tanonaka
authors.forename: H
authors.initials: H
authors.lastname: Yoshida
authors.forename: W
authors.initials: W
authors.lastname: Toga
authors.forename: K
authors.initials: K
authors.lastname: Furuhama
authors.forename: S
authors.initials: S
authors.lastname: Takeo
mesh_terms: D000818:Animals; D002352:Carrier Proteins / Q000378:metabolism; D018834:Chaperonin 60 / Q000378:metabolism; D003331:Coronary Vessels; D004195:Disease Models, Animal; D050883:HSC70 Heat-Shock Proteins; D055551:HSP27 Heat-Shock Proteins; D018840:HSP70 Heat-Shock Proteins; D050884:HSP72 Heat-Shock Proteins; D018841:HSP90 Heat-Shock Proteins / Q000378:metabolism; D006333:Heart Failure / Q000209:etiology* / Q000378:metabolism*; D006360:Heat-Shock Proteins / Q000096:biosynthesis* / Q000378:metabolism; D008026:Ligation; D008297:Male; D009203:Myocardial Infarction / Q000150:complications / Q000378:metabolism / Q000473:pathology; D009206:Myocardium / Q000378:metabolism*; D009363:Neoplasm Proteins / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
chemical_list: D002352:Carrier Proteins; D018834:Chaperonin 60; D050883:HSC70 Heat-Shock Proteins; D055551:HSP27 Heat-Shock Proteins; D018840:HSP70 Heat-Shock Proteins; D050884:HSP72 Heat-Shock Proteins; D018841:HSP90 Heat-Shock Proteins; D006360:Heat-Shock Proteins; C494373:Hspa8 protein, rat; C486114:Hspb1 protein, rat; D009363:Neoplasm Proteins