Bcl-xL inhibits different apoptotic pathways in rat PC12 cells

被引：20

作者：

Lindenboim, L ^{[1
]}

Haviv, R ^{[1
]}

Stein, R ^{[1
]}

机构：

[1] Tel Aviv Univ, George S Wise Fac Life Sci, Dept Neurobiochem, IL-69978 Ramat Aviv, Israel

来源：

NEUROSCIENCE LETTERS | 1998年 / 253卷 / 01期

基金：

以色列科学基金会;

关键词：

Bcl-x(L); apoptosis; PC12; cells; TNF alpha; caspases;

D O I：

10.1016/S0304-3940(98)00602-8

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Bcl-x(L,) a member of the bcl-2 family of proteins is required for the survival of neurons early in development. To study the mechanism of action of Bcl-x(L) in a neuronal context, we generated rat PC12 cells overexpressing Bcl-x(L) and examined their susceptibility to apoptotic stimuli that induce apoptosis through different pathways involving trophic-factor deprivation, staurosporine, tumor necrosis factor alpha or cisplatin. Overexpression of Bcl-x(L) in both naive and neuronal PC12 cells inhibited apoptosis induced by the different pathways. However, the extent of this protective effect varied, suggesting that the contribution of the Bcl-x(L)-controlled step to apoptosis differs in the different pathways. Our findings also showed that TNF alpha-induced activation of caspase-3 is inhibited by overexpression of Bcl-x(L), suggesting that Bcl-x(L) acts upstream of caspase activation. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：37 / 40

页数：4

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