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原癌基因bcl-2抑制PC12细胞中的细胞凋亡。

The protooncogene bcl-2 inhibits apoptosis in PC12 cells.

作者信息

Mah S P, Zhong L T, Liu Y, Roghani A, Edwards R H, Bredesen D E

机构信息

Department of Neurology, UCLA School of Medicine 90024-1769.

出版信息

J Neurochem. 1993 Mar;60(3):1183-6. doi: 10.1111/j.1471-4159.1993.tb03275.x.

Abstract

During development, many neuronal populations undergo a process of normal, programmed cell death, or apoptosis. Trophic factors regulate this process, but the mechanism by which they suppress apoptosis remains unclear. In the immune system, recent studies have implicated the protooncogene bcl-2 in the lymphocyte survival response to growth factors. To determine whether a similar survival pathway exists in a neuroendocrine cell type, we have expressed bcl-2 in the rat pheochromocytoma PC12 cell line and found that it abrogates the requirement for stimulation by growth factors to survive. bcl-2 expression also substantially delays the onset of injury by the calcium ionophore A23187.

摘要

在发育过程中,许多神经元群体经历正常的程序性细胞死亡或凋亡过程。营养因子调节这一过程,但其抑制凋亡的机制仍不清楚。在免疫系统中,最近的研究表明原癌基因bcl-2参与淋巴细胞对生长因子的存活反应。为了确定在神经内分泌细胞类型中是否存在类似的存活途径,我们在大鼠嗜铬细胞瘤PC12细胞系中表达了bcl-2,发现它消除了生长因子刺激以维持存活的需求。bcl-2的表达也显著延迟了钙离子载体A23187所致损伤的发生。

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