Bechtold D A, Brown I R
Department of Zoology, University of Toronto at Scarborough, 1265 Military Trail, West Hill, Toronto, Ontario, Canada.
Brain Res Mol Brain Res. 2000 Feb 22;75(2):309-20. doi: 10.1016/s0169-328x(99)00323-x.
Stressful stimuli activate the heat shock (stress) response in which a set of heat shock proteins (hsps) is induced, which play roles in cellular repair and protective mechanisms. Most studies in the mammalian nervous system have focused on Hsp70, however, the present investigation targets other members of the induced set, namely Hsp27 and Hsp32. In response to hyperthermia, these hsps are strongly induced in Bergmann glial cells in the rat brain and transported into their radial fibers, which project into the 'synaptic-enriched' molecular layer of the cerebellum. Using subcellular fractionation and immunoelectron microscopy, hyperthermia-induced Hsp27 and Hsp32 were detected in synaptic elements and in perisynaptic glial processes. These results suggest that stress-induced Hsp27 and Hsp32 may contribute to repair and protective mechanisms at the synapse.
应激刺激会激活热休克(应激)反应,在此反应中会诱导出一组热休克蛋白(Hsps),这些蛋白在细胞修复和保护机制中发挥作用。大多数关于哺乳动物神经系统的研究都集中在Hsp70上,然而,本研究的目标是诱导出的这组蛋白中的其他成员,即Hsp27和Hsp32。在对热疗的反应中,这些热休克蛋白在大鼠大脑的伯格曼胶质细胞中被强烈诱导,并被转运到它们的放射状纤维中,这些纤维伸向小脑的“富含突触”的分子层。通过亚细胞分级分离和免疫电子显微镜技术,在突触元件和突触周围的胶质细胞突起中检测到热疗诱导的Hsp27和Hsp32。这些结果表明,应激诱导的Hsp27和Hsp32可能有助于突触处的修复和保护机制。