72-kDa heat shock protein and mRNA expression after controlled cortical impact injury with hypoxemia in rats
72-kDa heat shock protein and mRNA expression after controlled cortical impact injury with hypoxemia in rats
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DOI：
10.1089/neu.1998.15.171
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发表时间：
1998-03-01
影响因子：
4.2
通讯作者：
Graham, SH
中科院分区：
文献类型：
--
作者：
Chen, MZ;Clark, RSB;Graham, SH
作为应激反应的一部分，缺血性和创伤性脑损伤（TBI）后在神经元中诱导72 kDa热休克蛋白（hsp 72）。为了研究TBI二次损伤后的应激反应，我们检测了大鼠控制性皮质撞击（CCI）损伤后继发性低氧血症和轻度低血压的区域和细胞hsp 72 mRNA和蛋白的表达。在创伤后6、8、24、72或168 h处死大鼠。将未处理和假手术大鼠用作对照。取脑，进行hsp 72的原位杂交（n = 2/组）、免疫细胞化学（n = 4/组）和Western印迹分析（n = 3至5/组）。Hsp 72 mRNA在海马CA 3区、海马门区和齿状回的神经元中表达。Hsp 72 mRNA主要表达在同侧皮质，在24小时，72小时Hsp 72 mRNA表达恢复到接近基础水平。Hsp 72蛋白在24 h可见于同侧皮质神经元、门神经元和海马CA 3区内侧面（CA 3-c）神经元。在72小时，热休克蛋白72免疫反应性降低，与24小时在这些相同的区域，但它是增加与基线。蛋白质印迹分析证实了在同侧皮质中hsp 72蛋白的增加。神经元中hsp 72 mRNA诱导的区域模式与CCI后蛋白表达的模式相似，除了hsp 72 mRNA而不是蛋白在海马CA 3区（CA 3-a）的齿状回和侧面表达。应激反应，如检测到的热休克蛋白72的表达，诱导在某些区域的一些神经元，选择性地容易受到迟发性神经元死亡在这个模型中的TBI。包括热休克蛋白72在内的一些蛋白的翻译失败可能与TBI后海马某些区域的迟发性神经元死亡有关。
As part of the stress response, the 72 kDa heat shack protein (hsp72) is induced in neurons after ischemic and traumatic brain injury (TBI). To examine the stress response after TBI with secondary insult, we examined the regional and cellular expression of hsp72 mRNA and protein after controlled cortical impact (CCI) injury with secondary hypoxemia and mild hypotension in rats. Rats were killed at 6, 8, 24, 72, or 168 h after trauma. Naive and sham-operated rats were used as controls. Brains were removed, and in situ hybridization (n = 2/group), immunocytochemistry (n = 4/group), and Western blot analysis (n = 3 to 5/group) for hsp72 was performed. Hsp72 mRNA was expressed in neurons in the ipsilateral cortex, CA3 region of the hippocampus, hilus, and dentate gyrus at 6 h. Hsp72 mRNA was expressed primarily in the ipsilateral cortex, at 24 h, and by 72 h hsp72 mRNA expression returned to near basal levels. Hsp72 protein was seen in ipsilateral cortical neurons, hilar neurons, and neurons in the medial aspect of the CA3 region of the hippocampus (CA3-c) at 24 h. At 72 h, hsp72 immunoreactivity was reduced versus 24 h in these same regions, but it was increased versus baseline. Western blot analysis confirmed an increase in hsp72 protein in the ipsilateral cortex. The regional pattern of hsp72 mRNA induction in neurons was similar to the pattern of protein expression after CCI, with the exceptions that hsp72 mRNA, but not protein, was expressed in the dentate gyrus and the lateral aspect of the CA3 region of the hippocampus (CA3-a). The stress response, as detected by hsp72 expression, is induced in some neurons in some regions that are selectively vulnerable to delayed neuronal death in this model of TBI. The failure to translate some proteins including hsp72 may be associated with delayed neuronal death in certain hippocampal regions after TBI.