Cheng Y F, Sun J R, Chen H B, Abdelnasir A, Tang S, Kemper N, Hartung J, Bao E D
College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.
Institute for Animal Hygiene, Animal Welfare and Farm Animal Behaviour, University of Veterinary Medicine Hannover, Foundation, Hannover, Germany.
Genet Mol Res. 2014 Nov 11;13(4):9371-81. doi: 10.4238/2014.November.11.3.
To investigate the protective role of Hsp60 against stress damage and its role in the sudden death of stressed animals, changes in the levels of Hsp60 protein and hsp60 mRNA of myocardial cells in vivo and in vitro were studied. In addition, the relationship between Hsp60 expression and heat-induced damage was also studied. Rats were exposed to a temperature of 42° ± 1°C for 0, 20, 40, 60, 80, or 100 min. More than 50% of the rats died suddenly within 100 min. With increasing heat stress duration, hsp60 mRNA levels significantly increased in both in vivo and in vitro rat myocardial cells; however, a similar trend was not observed for Hsp60 protein levels. Although the changes observed in Hsp60 expression in myocardial cells in vitro were inconsistent with those of rat heart tissues in vivo, Hsp60 expression levels were consistent with the histopathological damage observed in myocardial cells both in vivo and in vitro. Differences in Hsp60 expression may reflect the degree of injury sustained by myocardial cells in vivo and in vitro. As a mitochondrial protein, Hsp60 represents a potential biomarker of heat stress, and may protect against heat stress induced myocardial cellular damage both in vivo and in vitro.
为研究热休克蛋白60（Hsp60）对应激损伤的保护作用及其在应激动物猝死中的作用，我们研究了体内和体外心肌细胞中Hsp60蛋白水平及hsp60 mRNA的变化。此外，还研究了Hsp60表达与热诱导损伤之间的关系。将大鼠暴露于42°±1°C的温度下0、20、40、60、80或100分钟。超过50%的大鼠在100分钟内突然死亡。随着热应激持续时间的增加，体内和体外大鼠心肌细胞中的hsp60 mRNA水平均显著升高；然而，Hsp60蛋白水平未观察到类似趋势。尽管体外心肌细胞中Hsp60表达的变化与体内大鼠心脏组织的变化不一致，但Hsp60表达水平与体内和体外心肌细胞中观察到的组织病理学损伤一致。Hsp60表达的差异可能反映了体内和体外心肌细胞所遭受的损伤程度。作为一种线粒体蛋白，Hsp60代表了热应激的潜在生物标志物，并且可能在体内和体外保护心肌细胞免受热应激诱导的损伤。
