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首页> 外文期刊>Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism >Overexpression of HDJ-2 Protects Astrocytes from Ischemia-Like Injury and Reduces Redistribution of Ubiquitin Staining in Vitro.
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Overexpression of HDJ-2 Protects Astrocytes from Ischemia-Like Injury and Reduces Redistribution of Ubiquitin Staining in Vitro.

机译：HDJ-2的过表达保护星形胶质细胞免受缺血样损伤，并减少泛素染色的体外再分布。

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SUMMARY: HDJ-2, a member of the HSP40 family, functions as a cochaperone to promote protein folding both by binding to unfolded polypeptides and by regulating the activity of HSP70. This study tested whether HDJ-2 overexpression alone could provide significant protection from ischemia-like injury. Primary mouse astrocyte cultures were infected with an HDJ-2 encoding retroviral vector or control retrovirus lacking HDJ-2. Expression of HDJ-2 was confirmed by immunohistochemical staining and immunoblotting. Injury paradigms to mimic ischemia were glucose deprivation (GD) for 24 hours and oxygen-glucose deprivation (OGD) for 8 hours. Cell death was determined by trypan blue exclusion and cell counting. Overexpression of HDJ-2 alone significantly reduced astrocyte injury after both GD and OGD, independent of an elevation in HSP70. To further search for the mechanism of HDJ-2 protection, cultured astrocytes allowed to recover 16 hours after 8 hours GD were labeled with a monoclonal antiubiquitin antibody that recognizes both free ubiquitin and ubiquitinated proteins. The immunolabeling pattern changed from a relatively even distribution in both nuclei and cytoplasm in control cells to heterogeneous aggregates and marked reduction of nuclear staining in most of the cells after GD. When HDJ-2 was overexpressed, the number of cells with evidence of protein aggregation was significantly reduced. Thus, blocking protein aggregation may be an important mechanism by which HDJ-2 protects cells from damage.
机译：概述：HDJ-2是HSP40家族的成员，通过与未折叠的多肽结合并通过调节HSP70的活性，充当了陪伴蛋白来促进蛋白质折叠。这项研究测试了仅HDJ-2的过表达是否可以提供明显的保护，以免于缺血样损伤。用编码HDJ-2的逆转录病毒载体或缺乏HDJ-2的对照逆转录病毒感染原代小鼠星形胶质细胞。通过免疫组织化学染色和免疫印迹证实了HDJ-2的表达。模拟缺血的损伤范例是葡萄糖剥夺（GD）24小时和氧葡萄糖剥夺（OGD）8小时。通过锥虫蓝排除和细胞计数来确定细胞死亡。单独的HDJ-2的过表达显着减少了GD和OGD后星形胶质细胞的损伤，而与HSP70的升高无关。为了进一步寻找HDJ-2保护的机制，在GD处理8小时后允许恢复16小时的星形胶质细胞用单克隆抗泛素抗体标记，该抗体可识别游离泛素和泛素蛋白。免疫标记模式从对照细胞的核和细胞质中相对均匀的分布改变为异质聚集体，GD后大多数细胞的核染色明显减少。当HDJ-2过表达时，具有蛋白质聚集迹象的细胞数量显着减少。因此，阻断蛋白质聚集可能是HDJ-2保护细胞免受损害的重要机制。

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