Che-1, a recently identified apoptosis related protein, affects the fate of various cell types when under stress. One attractive biological function of Che-1 is promoting the transcription of p53 after DNA damage; besides, it can also regulate cell cycle via interacting with retinoblastoma protein. Although previous evidence has showed its anti-apoptotic role in cancer cells, some studies point out that Che-1 might play an opposite role in central nervous system (CNS). However, the function of Che-1 in CNS is still with limited acquaintance. To investigate whether Che-1 is involved in CNS lesion, we performed a traumatic brain injury model in adult rats. Up-regulation of Che-1 was observed in the peritrauma brain cortex by performing western blotting and immunohistochemistry. Terminal deoxynucleotidyl transferase deoxy-UTP nick-end labeling and 4',6-diamidino-2-phenylindole staining suggested that Che-1 was involved in neuronal apoptosis after brain injury. We also investigated co-localization of Che-1 and active-caspase-3 in the ipsilateral brain cortex. In addition, the expression patterns of p53, Bax and PCNA were parallel with that of Che-1. Besides this, neurotrophin receptor-interacting MAGE homolog was found to be associated with Che-1 after brain trauma. Based on our data, we suggested that Che-1 might play an important role in neuronal apoptosis following TBI; and might provide a basis for the further study on its role in regulating the expression of p53 and cell cycle re-entry in traumatic brain injury.

译文

:Che-1是最近发现的凋亡相关蛋白,在压力下会影响各种细胞类型的命运。 Che-1的一种有吸引力的生物学功能是促进DNA损伤后p53的转录。此外,它还可以通过与视网膜母细胞瘤蛋白相互作用来调节细胞周期。尽管先前的证据表明其在癌细胞中具有抗凋亡作用,但一些研究指出,Che-1可能在中枢神经系统(CNS)中起相反的作用。但是,Che-1在中枢神经系统中的功能仍知之甚少。为了研究Che-1是否参与中枢神经系统病变,我们在成年大鼠中进行了脑外伤模型。通过进行蛋白质印迹和免疫组织化学观察,在创伤周围大脑皮层中观察到Che-1的上调。末端脱氧核苷酸转移酶脱氧-UTP缺口末端标记和4',6-二mid基-2-苯基吲哚染色提示Che-1参与脑损伤后的神经元凋亡。我们还研究了同侧大脑皮层中Che-1和active-caspase-3的共定位。另外,p53,Bax和PCNA的表达模式与Che-1平行。除此之外,还发现与神经营养蛋白受体相互作用的MAGE同源物与脑外伤后的Che-1有关。根据我们的数据,我们认为Che-1可能在TBI后的神经元凋亡中起重要作用。可能为进一步研究其在创伤性脑损伤中调控p53表达和细胞周期再进入的作用提供基础。

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