This result indicates an up regulation of HSP60 in response to chronic atrial fibrillation.

The increased expression of mortalin may represent an adaptive heat shock response to restore cellular homeostasis.

No abstract

Introduction: Cardiomyocytes respond to stress with the expression of various heat shock proteins (HSPs). Expression of mitochondrial HSP60 is known to be induced by various stress factors, including ischaemia and reperfusion. The aim of the study was to investigate the induction of HSP60 in human myocardium during cardiac surgery. Method: From eight patients undergoing elective coronary artery bypass grafting or valve replacement, samples of right atrium were harvested before and after extracorporeal circulation (ECC). Two patients had atrial fibrillation and six were in sinus rhythm. The myocardial samples were excised and immediately immersed in liquid nitrogen. The HSP60 protein level was determined using sodium dodecyl sulphate-polyacryl-amide gel electrophoresis, Western blot, and subsequent ECL technique. The amount of HSP60 protein was quantified by optical densitometry, according to the immunoreactive bands of actin. Results: In all samples HSP60 was detected before and after ECC. We could not find any difference in HSP60 expression before and during cardiac surgery. There was no correlation with duration of cardiopulmonary bypass or reperfusion time. Conclusion: We could not demonstrate a cytoprotective upregulation of HSP60 after an obligatory period of ischaemia, cardioplegic arrest and reperfusion. This might reflect effective cardioprotection during ECC.