Kawagoe J, Abe K, Kogure K
Department of Neurology, Institute of Brain Diseases, Tohoku University School of Medicine, Sendai, Japan.
Neurosci Lett. 1993 Apr 30;153(2):165-8. doi: 10.1016/0304-3940(93)90313-a.
Induction of heat shock protein (HSP) 70 and heat shock cognate protein (HSC) 70 mRNAs, and immunoreactivity for HSP70 were investigated in rat hippocampus after transient global ischemia with in situ hybridization and immunohistochemistry. In sham control brain, HSP70 mRNA was scarcely present, while HSC70 mRNA was expressed in most neuronal cells. After 20 min of transient four-vessel occlusion (4VO), ischemia-resistant hippocampal CA3 cells consistently induced HSP70 mRNA along with further HSC70 mRNA. The resistant dentate granule (DG) cells continuously induced HSC70 mRNA even after the great reduction of HSP70 mRNA. In contrast, in ischemia-vulnerable CA1 cells, a relatively lower level of HSC70 mRNA induction than the level of HSP70 mRNA induction was observed. The vulnerable CA1 cells produced a prominent HSP70 immunoreactivity. These results suggest that the vulnerability of the CA1 cells after transient ischemia may not be explained only by the ability of HSP70 induction, but may be related to the imbalance of HSP70 and HSC70 mRNA inductions.
采用原位杂交和免疫组化方法，研究了短暂性全脑缺血后大鼠海马中热休克蛋白（HSP）70和热休克同源蛋白（HSC）70 mRNA的诱导情况以及HSP70的免疫反应性。在假手术对照脑中，HSP70 mRNA几乎不存在，而HSC70 mRNA在大多数神经细胞中表达。短暂性四动脉闭塞（4VO）20分钟后，抗缺血的海马CA3细胞持续诱导HSP70 mRNA，同时HSC70 mRNA进一步增加。即使HSP70 mRNA大幅减少，抗缺血的齿状颗粒（DG）细胞仍持续诱导HSC70 mRNA。相比之下，在易缺血的CA1细胞中，观察到HSC70 mRNA的诱导水平相对低于HSP70 mRNA的诱导水平。易缺血的CA1细胞产生了显著的HSP70免疫反应性。这些结果表明，短暂性缺血后CA1细胞的易损性可能不能仅通过HSP70的诱导能力来解释，而可能与HSP70和HSC70 mRNA诱导的失衡有关。
