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

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 cardi...

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Veröffentlicht in:The Annals of thoracic surgery 2002-09, Vol.74 (3), p.767-770
Hauptverfasser: Schäfler, Alfons E, Kirmanoglou, Kiriakos, Pecher, Peter, Hannekum, Andreas, Schumacher, Bernd
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container_issue 3
container_start_page 767
container_title The Annals of thoracic surgery
container_volume 74
creator Schäfler, Alfons E
Kirmanoglou, Kiriakos
Pecher, Peter
Hannekum, Andreas
Schumacher, Bernd
description 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.
doi_str_mv 10.1016/S0003-4975(02)03830-4
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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.</description><identifier>ISSN: 0003-4975</identifier><identifier>EISSN: 1552-6259</identifier><identifier>DOI: 10.1016/S0003-4975(02)03830-4</identifier><identifier>PMID: 12238837</identifier><identifier>CODEN: ATHSAK</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Aged ; Atrial Fibrillation - pathology ; Biological and medical sciences ; Blotting, Western ; Cardiac dysrhythmias ; Cardiology. 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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.</description><subject>Aged</subject><subject>Atrial Fibrillation - pathology</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Cardiac dysrhythmias</subject><subject>Cardiology. 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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. 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subjects Aged
Atrial Fibrillation - pathology
Biological and medical sciences
Blotting, Western
Cardiac dysrhythmias
Cardiology. Vascular system
Chaperonin 10 - metabolism
Chaperonin 60 - metabolism
Chronic Disease
Electrophoresis, Polyacrylamide Gel
Female
Heart
Heart Atria - pathology
Humans
Male
Medical sciences
Middle Aged
Mitochondria, Heart - pathology
Myocardium - pathology
Reference Values
Up-Regulation - physiology
title Overexpression of heat shock protein 60/10 in myocardium of patients with chronic atrial fibrillation
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