Temporal Profiles of Stress Protein Inductions after Focal Transient Ischemia in Mice Brain.
Temporal Profiles of Stress Protein Inductions after Focal Transient Ischemia in Mice Brain.
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DOI：
10.1016/j.jstrokecerebrovasdis.2016.05.031
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发表时间：
2016-10
期刊：
影响因子：
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通讯作者：
Qian Li;Y. Nakano;Jingwei Shang;Y. Ohta;Kota Sato;M. Takemoto;N. Hishikawa;T. Yamashita;K. Abe
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文献类型：
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作者：
Qian Li;Y. Nakano;Jingwei Shang;Y. Ohta;Kota Sato;M. Takemoto;N. Hishikawa;T. Yamashita;K. Abe
应激蛋白在缺氧、氧化、热休克和蛋白酶体应激下对缺血性脑损伤具有重要的保护作用。方法在再灌注后7天内，观察小鼠脑内缺氧诱导因子-1α (HIF-1α)、谷胱甘肽（GSH）、热休克蛋白72 （HSP72）、构成性热休克同源蛋白73 （HSC73）、泛素等主要应激蛋白在短暂性大脑中动脉闭塞45分钟后的时间变化。结果HIF-1α、GSH、HSP72和泛素的免疫组化分析显示，假对照脑神经细胞的免疫反应性较弱，而HSC73的免疫反应性较强。tcao后缺血周围区HSC73在12 h时升高最快，HIF-1α在24 h时达到峰值，GSH、HSP72和泛素在72 h达到峰值。直到第7天，所有这些应激蛋白都恢复到基线水平。在缺血核心，这些应激蛋白表现出类似的变化，与缺血周围区域相比，反应更少。结论这些数据显示了tMCAO后小鼠脑内HIF-1α、GSH、HSP72、HSC73和泛素在时间上的表达，可能为进一步了解脑缺血性疾病的神经保护机制和治疗干预提供新的靶点。
BackgroundStress proteins have been found to play important protective roles against ischemic brain injury under hypoxic, oxidative, heat shock, and proteasome stresses.MethodsIn the present study, we investigated the temporal profiles of the major stress proteins including hypoxia-inducible factor-1α (HIF-1α), glutathione (GSH), heat shock protein 72 (HSP72), constitutive heat shock cognate protein 73 (HSC73), and ubiquitin after 45 minutes of transient middle cerebral artery occlusion (tMCAO) in the mice brain up to 7 days after reperfusion.ResultsImmunohistochemical analyses of HIF-1α, GSH, HSP72, and ubiquitin showed little immunoreactivity of neural cells in sham control brain, whereas HSC73 showed a constitutive immunoreactivity. After tMCAO, HSC73 showed the fastest increase at 12 hours in the peri-ischemic area, followed by HIF-1α with a peak at 24 hours, GSH, HSP72, and ubiquitin with a peak at 72 hours. All these stress proteins returned toward the baseline levels until 7 days. In the ischemic core, these stress proteins showed a similar change with less reaction compared to the peri-ischemic area.ConclusionsThese data showed temporal expressions of HIF-1α, GSH, HSP72, HSC73, and ubiquitin in the mice brain after tMCAO, which might provide a better understanding of neuroprotective mechanisms and novel targets for therapeutic intervention of brain ischemic disease.