热休克蛋白70（HSP70）的神经保护潜力。

The neuroprotective potential of heat shock protein 70 (HSP70).

作者信息

Yenari M A, Giffard R G, Sapolsky R M, Steinberg G K

机构信息

Departments of Neurosurgery, Neurology and Stanford Stroke Center, Stanford University Medical Center, Stanford University, Stanford, CA 94305, USA.

出版信息

Mol Med Today. 1999 Dec;5(12):525-31. doi: 10.1016/s1357-4310(99)01599-3.

DOI:10.1016/s1357-4310(99)01599-3

PMID:10562718

Abstract

In response to many metabolic disturbances and injuries, including stroke, neurodegenerative disease, epilepsy and trauma, the cell mounts a stress response with induction of a variety of proteins, most notably the 70-kDa heat shock protein (HSP70). Whether stress proteins are neuroprotective has been hotly debated, as these proteins might be merely an epiphenomenon unrelated to cell survival. Only recently, with the availability of transgenic animals and gene transfer, has it become possible to overexpress the gene encoding HSP70 to test directly the hypothesis that stress proteins protect cells from injury. A few groups have now shown that overproduction of HSP70 leads to protection in several different models of nervous system injury. This review will cover these studies, along with the potential mechanisms by which HSP70 might mediate cellular protection.

摘要

针对包括中风、神经退行性疾病、癫痫和创伤在内的许多代谢紊乱和损伤，细胞会通过诱导多种蛋白质产生应激反应，其中最显著的是70 kDa热休克蛋白（HSP70）。应激蛋白是否具有神经保护作用一直备受争议，因为这些蛋白可能仅仅是与细胞存活无关的一种附带现象。直到最近，随着转基因动物和基因转移技术的出现，才有可能通过过表达编码HSP70的基因来直接检验应激蛋白保护细胞免受损伤这一假说。现在有几个研究小组表明，在几种不同的神经系统损伤模型中，HSP70的过量产生都能起到保护作用。本综述将涵盖这些研究，以及HSP70可能介导细胞保护的潜在机制。