Behl C, Hovey L, Krajewski S, Schubert D, Reed J C
Salk Institute for Biological Studies, La Jolla, CA 92037.
Biochem Biophys Res Commun. 1993 Dec 15;197(2):949-56. doi: 10.1006/bbrc.1993.2571.
The 26-kDa protein encoded by the bcl-2 gene is a regulator of cell survival and blocks cell death induced by numerous stimuli. Amyloid beta protein (ABP) and glutamate are believed to play important roles in the neuronal cell death that occurs in Alzheimer's disease and stroke, respectively. Glutamate induces apoptosis in some neuronal cell systems, but it remains controversial whether ABP-mediated cell death occurs through apoptosis or necrosis. To further explore the pathways for cell death that are activated by these neurotoxins, we examined the effects of elevated levels of the p26-Bcl-2 protein on the susceptibility of neuronal cell lines to killing by glutamate and ABP. Gene transfer methods were used to elevate p26-Bcl-2 protein levels in the rat nerve lines PC-12 and B50 and the human neuroblastoma IMR-5. Bcl-2 protected all 3 cell lines from glutamate induced cell death but had no effect on killing mediated by ABP.
由bcl - 2基因编码的26 kDa蛋白是细胞存活的调节因子，可阻止多种刺激诱导的细胞死亡。据信，β-淀粉样蛋白（ABP）和谷氨酸分别在阿尔茨海默病和中风中发生的神经元细胞死亡中起重要作用。谷氨酸在一些神经元细胞系统中诱导细胞凋亡，但ABP介导的细胞死亡是通过凋亡还是坏死发生仍存在争议。为了进一步探索这些神经毒素激活的细胞死亡途径，我们研究了p26 - Bcl - 2蛋白水平升高对神经元细胞系对谷氨酸和ABP杀伤敏感性的影响。采用基因转移方法提高大鼠神经细胞系PC - 12和B50以及人神经母细胞瘤IMR - 5中p26 - Bcl - 2蛋白水平。Bcl - 2保护所有3种细胞系免受谷氨酸诱导的细胞死亡，但对ABP介导的杀伤没有影响。
