Yoon S O, Casaccia-Bonnefil P, Carter B, Chao M V
Department of Biological Sciences, Columbia University, New York, New York 10027, USA.
J Neurosci. 1998 May 1;18(9):3273-81. doi: 10.1523/JNEUROSCI.18-09-03273.1998.
In addition to its role as a survival factor, nerve growth factor (NGF) has been implicated in initiating apoptosis in restricted cell types both during development and after terminal cell differentiation. NGF binds to the TrkA tyrosine kinase and the p75 neurotrophin receptor, a member of the tumor necrosis factor cytokine family. To understand the mechanisms underlying survival versus death decisions, the TrkA receptor was introduced into oligodendrocyte cell cultures that undergo apoptosis in a p75-dependent manner. Here we report that activation of the TrkA NGF receptor in oligodendrocytes negates cell death by the p75 receptor. TrkA-mediated rescue from apoptosis correlated with mitogen-activated protein kinase activation. Concurrently, activation of TrkA in oligodendrocytes resulted in suppression of c-jun kinase activity initiated by p75, whereas induction of NFkappaB activity by p75 was unaffected. These results indicate that TrkA-mediated rescue involves not only activation of survival signals but also simultaneous suppression of a death signal by p75. The selective interplay between tyrosine kinase and cytokine receptors provides a novel mechanism that achieves alternative cellular responses by merging signals from different ligand-receptor systems.
除了作为一种生存因子发挥作用外,神经生长因子(NGF)在发育过程中和终末细胞分化后,还参与启动特定细胞类型的凋亡。NGF与TrkA酪氨酸激酶以及p75神经营养因子受体结合,p75神经营养因子受体是肿瘤坏死因子细胞因子家族的成员。为了理解生存与死亡决定背后的机制,将TrkA受体导入以p75依赖方式发生凋亡的少突胶质细胞培养物中。在此我们报告,少突胶质细胞中TrkA NGF受体的激活可消除p75受体介导的细胞死亡。TrkA介导的对凋亡的挽救与丝裂原活化蛋白激酶的激活相关。同时,少突胶质细胞中TrkA的激活导致由p75引发的c-jun激酶活性受到抑制,而p75对NFκB活性的诱导则不受影响。这些结果表明,TrkA介导的挽救不仅涉及生存信号的激活,还同时抑制了p75的死亡信号。酪氨酸激酶和细胞因子受体之间的选择性相互作用提供了一种新机制,通过整合来自不同配体-受体系统的信号来实现不同的细胞反应。