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热休克和运动后大鼠心脏中热休克转录因子的激活

Activation of heat-shock transcription factor in rat heart after heat shock and exercise.

作者信息

Locke M, Noble E G, Tanguay R M, Feild M R, Ianuzzo S E, Ianuzzo C D

机构信息

Deborah Research Institute, Browns Mills, New Jersey 08015-1799, USA.

出版信息

Am J Physiol. 1995 Jun;268(6 Pt 1):C1387-94. doi: 10.1152/ajpcell.1995.268.6.C1387.

Abstract

Stress-induced transcriptional regulation of the heat-shock proteins (HSP) is mediated by activation and binding of the heat-shock transcription factors (HSF) to the heat-shock element (HSE). Given the similarities between the stressors known to activate the HSF in cultured cells and the physiological stresses known to occur during exercise, HSF activation was examined in the hearts from exercising animals. Sprague-Dawley rats (5 rats/group) were run on a treadmill (24 m/min) for either 0, 20, 40, or 60 min or to exhaustion (102 +/- 7 min). Protein extracts were assessed for HSF activation by mobility-shift gels. Extracts from the hearts of nonrunning rats demonstrated no HSF activation, whereas HSF activation was detected in 80% of the hearts from animals that run for at least 40 min. These results demonstrate that treadmill running is capable of activating the HSF and increasing 70-kDa HSP mRNA in the rat myocardium.

摘要

应激诱导的热休克蛋白(HSP)转录调控是由热休克转录因子(HSF)激活并结合到热休克元件(HSE)介导的。鉴于已知在培养细胞中激活HSF的应激源与已知在运动过程中发生的生理应激之间存在相似性,我们检测了运动动物心脏中的HSF激活情况。将斯普拉格-道利大鼠(每组5只大鼠)在跑步机上以24米/分钟的速度跑0、20、40或60分钟,或直至力竭(102±7分钟)。通过迁移率变动凝胶分析蛋白质提取物的HSF激活情况。未跑步大鼠心脏的提取物未显示HSF激活,而在至少跑了40分钟的动物心脏中,80%检测到HSF激活。这些结果表明,跑步机跑步能够激活大鼠心肌中的HSF并增加70 kDa HSP mRNA。

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