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Ann Thorac Surg 2002;74:767-770
© 2002 The Society of Thoracic Surgeons

Original article: cardiovascular

Overexpression of heat shock protein 60/10 in myocardium of patients with chronic atrial fibrillation

Alfons E. Schäfler, MD*a,b, Kiriakos Kirmanogloub, Peter Pecher, MDa,b, Andreas Hannekum, MDa, Bernd Schumacher, MDa,b

a Department of Cardiac Surgery, University of Ulm, Ulm, Germany
b Cardiovascular Research Center, University of Ulm, Ulm, Germany

Accepted for publication May 29, 2002.

* Address reprint requests to Dr Schäfler, Department of Cardiac Surgery and Cardiovascular Research Center, University of Ulm, Steinhövelstr. 9, 89075 Ulm, Germany
e-mail: aschaefler{at}gmx.de

Background. Cardiomyocytes respond to chronic atrial fibrillation with increased expression of heat shock protein 60 (HSP60). The aim of this study was to investigate whether expression of the coprotein HSP10 is also increased.

Methods. Right atrial samples from 16 patients undergoing elective cardiac operation were excised and immediately frozen in liquid nitrogen. Eight patients had chronic atrial fibrillation and 8 patients were in sinus rhythm. The HSP60 and HSP10 protein levels were determined by SDS-PAGE, Western blot, and quantified by optical densitometry according to the immunoreactive bands of actin.

Results. In myocardial samples from patients with chronic atrial fibrillation we found simultaneous upregulation of both stress proteins. HSP60 expression was more than 2.3-fold and HSP10 expression was more than 2.4-fold increased in atrial myocardium of patients with chronic atrial fibrillation.

Conclusions. These results indicate functional upregulation of mitochondrial HSP60 and HSP10 in response to chronic atrial fibrillation.




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[Abstract] [Full Text] [PDF]


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