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The role of HSPA12B in regulating neuronal apoptosis.

机译:HSPA12B在调节神经元细胞凋亡中的作用。

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摘要

Heat shock protein A12B (HSPA12B) is the newest member of a recently defined subfamily of proteins distantly related to the 70-kDa family of heat shock proteins (HSP70) family. HSP70s play a crucial role in protecting cells, tissues, organs and animals from various noxious conditions. Here we studied the dynamic expression changes and localization of HSPA12B after middle cerebral artery occlusion (MCAO) with reperfusion induced ischemic insult processes in adult rats. Apoptosis, as indicated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, was also increased in the peri-ischemic cortex compared to non-ischemic hemisphere. The expression of HSPA12B was strongly induced in the ischemic hemisphere of MCAO reperfusion rats in vivo. In vitro studies indicated that the up-regulation of HSPA12B may be involved in oxygen-glucose deprivation-induced PC12 cell death. And knockdown of HSPA12B in cultured differentiated PC12 cells by siRNA showed that HSPA12B inhibited the expression of active caspase-3. Collectively, these results suggested that HSPA12B may be required for protecting neurons from ischemic insults.
机译:热休克蛋白 A12B (HSPA12B) 是最近定义的蛋白质亚家族的最新成员,与 70-kDa 热休克蛋白 (HSP70) 家族远亲。HSP70 在保护细胞、组织、器官和动物免受各种有害条件的影响方面起着至关重要的作用。本文研究了成年大鼠大脑中动脉闭塞(MCAO)后HSPA12B的动态表达变化和定位,再灌注诱导了缺血性损伤过程。与非缺血半球相比,终末脱氧核苷酸转移酶 dUTP 缺口末端标记 (TUNEL) 染色表明的细胞凋亡在缺血周皮层中也有所增加。MCAO再灌注大鼠体内缺血半球强烈诱导HSPA12B表达。体外研究表明,HSPA12B的上调可能与氧葡萄糖剥夺诱导的 PC12 细胞死亡有关。通过siRNA敲除培养的分化PC12细胞中的HSPA12B表明HSPA12B抑制了活性caspase-3的表达。总的来说,这些结果表明,可能需要HSPA12B来保护神经元免受缺血性损伤。

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