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首页> 外文期刊>Cell and Tissue Research >TGF-β superfamily members, ActivinA and TGF-β1, induce apoptosis in oligodendrocytes by different pathways
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TGF-β superfamily members, ActivinA and TGF-β1, induce apoptosis in oligodendrocytes by different pathways

机译：TGF-β超家族成员ActivinA和TGF-β1通过不同途径诱导少突胶质细胞凋亡

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摘要

Activins and transforming growth factor (TGF)-βs, members of the TGF-β superfamily, affect numerous physiological processes, including apoptosis, in a variety of organs and tissues. Apoptotic functions of TGF-βs, in contrast to those of the activins, are well documented in the developing and adult nervous system. TGF-βs operate in a context-dependent manner and cooperate with other cytokines in the regulation of apoptosis. In this study, we show, for the first time, an apoptotic function of ActivinA in the nervous system, i.e. in oligodendroglial progenitor cells. Using the oligodendroglial cell line OLI-neu, we show that ActivinA acts autonomously, without cooperating with TGF-β. In contrast to the mechanism of TGF-β-mediated apoptosis involving Bcl-xl down-regulation, Bcl-xl in ActivinA-induced apoptosis is classically sequestered by the BH3-only protein Puma. Puma expression is controlled by the transcription factor p53 as demonstrated by experiments with the p53 inhibitor Pifithrin-α. Furthermore, in the apoptotic TGF-β pathway, caspase-3 is activated, whereas in the apoptotic ActivinA pathway, apoptosis-inducing factor is released to trigger DNA fragmentation. These data suggest that TGF-β and ActivinA induce apoptosis in oligodendrocytes by different apoptotic pathways.
机译：作为TGF-β超家族成员的激活素和转化生长因子（TGF）-β，会影响多种器官和组织的许多生理过程，包括细胞凋亡。与激活素相反，TGF-βs的凋亡功能在发育中的和成年的神经系统中有很好的记录。 TGF-β以上下文依赖的方式起作用，并与其他细胞因子协同调节细胞凋亡。在这项研究中，我们首次显示了激活素A在神经系统（即少突胶质祖细胞）中的凋亡功能。使用少突胶质细胞系OLI-neu，我们显示ActivinA自主发挥作用，而无需与TGF-β协同作用。与涉及Bcl-xl下调的TGF-β介导的细胞凋亡机制相反，激活素A诱导的细胞凋亡中的Bcl-xl经典地被仅BH3蛋白Puma隔离。如p53抑制剂Pifithrin-α的实验所示，Puma的表达受转录因子p53的控制。此外，在凋亡的TGF-β途径中，caspase-3被激活，而在凋亡的ActivinA途径中，凋亡诱导因子被释放以触发DNA片段化。这些数据表明，TGF-β和激活素A通过不同的凋亡途径诱导少突胶质细胞的凋亡。

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