Kirmanoglou Kiriakos, Hannekum Andreas, Schäfler Alfons E
Department of Cardiac Surgery, University of Ulm, Steinhövelstr. 9, 89075 Ulm, Germany.
Basic Res Cardiol. 2004 Nov;99(6):404-8. doi: 10.1007/s00395-004-0477-4. Epub 2004 May 5.
In myocardium of patients with chronic atrial fibrillation (AF) the expression of the mitochondrial heat shock proteins HSP60 and HSP10 is increased. They are responsible for folding and translocation of proteins inside the mitochondria. Import of these proteins is accomplished by mortalin. The aim of our study was to investigate if the expression of the heat shock protein mortalin is also increased in patients with AF.
Right atrial samples from 18 patients undergoing elective cardiac surgery were excised and immediately frozen in liquid nitrogen: 8 patients had chronic AF (> or = 3 month) and 10 patients were in sinus rhythm (SR). Mortalin was determined by SDS-PAGE, Western blot and quantified by optical densitometry.
In myocardial samples from patients with chronic AF we found a more than 2-fold increase in mortalin expression.
The increased expression of mortalin may represent an adaptive heat shock response to restore cellular homeostasis.
在慢性心房颤动(AF)患者的心肌中,线粒体热休克蛋白HSP60和HSP10的表达增加。它们负责线粒体内蛋白质的折叠和转运。这些蛋白质的导入由mortalin完成。我们研究的目的是调查AF患者中热休克蛋白mortalin的表达是否也增加。
从18例接受择期心脏手术的患者中切除右心房样本,并立即在液氮中冷冻:8例患者患有慢性AF(≥3个月),10例患者为窦性心律(SR)。通过SDS-PAGE、蛋白质印迹法测定mortalin,并通过光密度法进行定量。
在慢性AF患者的心肌样本中,我们发现mortalin表达增加了2倍以上。
mortalin表达增加可能代表一种适应性热休克反应,以恢复细胞内稳态。