全脑缺血后72-kDa热休克蛋白表达的时间变化情况。
The temporal profile of 72-kDa heat-shock protein expression following global ischemia.
作者信息
Simon R P, Cho H, Gwinn R, Lowenstein D H
机构信息
Department of Neurology, University of California, San Francisco 94143.
出版信息
J Neurosci. 1991 Mar;11(3):881-9. doi: 10.1523/JNEUROSCI.11-03-00881.1991.
The potential role of the nonconstitutive 72-kDa heat-shock protein (HSP72) in selective neuronal vulnerability to ischemia was studied in rats subjected to graded global ischemia. Immunocytochemistry using a monoclonal antibody against HSP72 was performed on tissue collected after 24 hr of reperfusion. The appearance of HSP72 immunoreactivity correlated in a graded fashion with those regions known to be selectively vulnerable in ischemia. That is, HSP72 was induced in only hilar interneurons and CA1 pyramidal cells following brief ischemia. After intermediate durations of ischemia, HSP72 was expressed in the CA3 neurons and cortical layers 3 and 5, and after the longest intervals, HSP72 appeared in dentate granule cells. Heat-shock protein expression preceded cell death (assessed with acid fuchsin staining) in all regions. This temporal profile suggests that the capability of neurons to express HSP72 is unlikely to account for selective vulnerability of different brain regions following ischemia; its role in neuroprotection during ischemic injury in vivo remains unknown.
在经历分级全脑缺血的大鼠中，研究了非组成型72-kDa热休克蛋白（HSP72）在神经元对缺血的选择性易损性中的潜在作用。在再灌注24小时后收集的组织上，使用抗HSP72单克隆抗体进行免疫细胞化学检测。HSP72免疫反应性的出现与已知在缺血中具有选择性易损性的区域呈分级相关。也就是说，短暂缺血后仅在海马门区中间神经元和CA1锥体细胞中诱导出HSP72。缺血持续时间中等时，HSP72在CA3神经元以及皮质第3和第5层中表达，而在最长缺血间隔后，HSP72出现在齿状颗粒细胞中。在所有区域，热休克蛋白表达都先于细胞死亡（用酸性品红染色评估）。这种时间特征表明，神经元表达HSP72的能力不太可能解释缺血后不同脑区的选择性易损性；其在体内缺血性损伤期间的神经保护作用仍然未知。
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