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. 2003;12(1):60-5.
doi: 10.1046/j.1444-2892.2003.00139.x.

Myocardial heat shock protein changes in the failing heart following coronary artery ligation

Kouichi Tanonaka  1 , Wakako Toga, Hiroyuki Yoshida, Satoshi Takeo
Affiliations

Myocardial heat shock protein changes in the failing heart following coronary artery ligation

Kouichi Tanonaka et al. Heart Lung Circ. 2003.

Abstract

Background: Production of several heat shock proteins (Hsp) is enhanced after exposure to stress. There is little information concerning changes in myocardial Hsp under pathophysiological conditions. The aim of this study was to determine alterations in Hsp content in the viable left ventricular myocardium during the development of heart failure following coronary artery ligation (CAL).

Methods: Myocardial infarction was produced by CAL of Wistar rats. One and eight weeks after the operation, haemodynamic parameters of rats with CAL were determined and then expression of Hsp27, Hsp60 and Hsp72 was measured by western blotting.

Results: Animals showed a decrease in cardiac output and an increase in left ventricular end-diastolic pressure, symptoms of chronic heart failure (CHF), 8 weeks after CAL. Myocardial Hsp27 and Hsp72 at 1 week after CAL significantly increased, whereas expression of both proteins at 8 weeks was similar to that in rats which underwent a sham operation (without coronary artery ligation). In contrast, Hsp60 at 8 weeks, but not at 1 week, significantly increased in the sham rats.

Conclusions: Diverse changes in myocardial Hsp occurred during the development of CHF.

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