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首页> 外文期刊>Cell biology international. >Role of c-Jun N-terminal kinase activation in apoptosis induced by removal of the growth factors
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Role of c-Jun N-terminal kinase activation in apoptosis induced by removal of the growth factors

机译：c-Jun N-末端激酶激活在去除生长因子诱导的凋亡中的作用

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Apoptosis plays a crucial role for generation of lymphocyte repertoire, clonal contraction, and elimination of virus-infected cells. Since IL-3-dependent pro-B cell line Baf-3 resulted in rapid induction of apoptotic cell death upon IL-3 withdrawal, it would by very valuable for analysis of apoptosis induction by growth factor deprivation. First, we confirmed that Baf-3 cells underwent loss of mitochondrial membrane potential (m) and apoptosis in a time-dependent manner when they were cultured in the RPMI-1640 medium without IL-3. Induction of apoptosis and loss of m was determined by DiOC6 and annexin V staining method using flow cytometer, respectively. Deprivation of IL-3 induced upregulation of proapoptotic molecule Bax, in conjunction with slight down-regulation of anti-apoptotic molecule Bcl-xL, which was assessed by Western blotting. Since Bcl-xL-overexpressing Baf-3 cells showed some resistance to IL-3-deprivation, Bcl-xL prevents apoptosis induced by IL-3 withdrawal. Finally, a sustained JNK1 activation was observed prior to induction of apoptosis upon IL-3 deprivation. Dominat-negative form of JNK1 and JNK inhibitor sp600125 partially inhibit the apoptosis upon IL-3 deprivation, suggesting that a sustained JNK1 activation was involved in the induction of apoptosis. Together, IL-3 deprivation of IL-3-dependent cell line Baf-3 induces a sustained JNK1 activation, followed by a decline of the ratio of Bcl-xL to Bax, leading to loss of m, and finally apoptosis.
机译：凋亡对于淋巴细胞库的产生，克隆收缩以及消除病毒感染的细胞起着至关重要的作用。由于依赖IL-3的pro-B细胞系Baf-3导致在IL-3撤药后迅速诱导凋亡细胞死亡，因此对于分析生长因子剥夺引起的凋亡诱导具有非常重要的意义。首先，我们证实，当Baf-3细胞在无IL-3的RPMI-1640培养基中培养时，它以时间依赖性的方式经历了线粒体膜电位（m）的丧失和细胞凋亡。使用流式细胞仪分别通过DiOC6和膜联蛋白V染色法测定凋亡诱导和m丢失。剥夺IL-3会诱导凋亡前分子Bax的上调，再加上抗凋亡分子Bcl-xL的下调，这是通过Western印迹法评估的。由于过表达Bcl-xL的Baf-3细胞对IL-3剥夺表现出一定的抵抗力，因此Bcl-xL可以防止IL-3撤药诱导的细胞凋亡。最后，在IL-3剥夺后诱导凋亡之前，观察到持续的JNK1活化。 JNK1和JNK抑制剂sp600125的负阴性形式部分抑制IL-3剥夺时的凋亡，这表明持续的JNK1激活与凋亡的诱导有关。在一起，IL-3依赖性细胞系Baf-3的IL-3剥夺诱导了持续的JNK1激活，随后Bcl-xL与Bax的比率下降，导致m丢失，最后导致细胞凋亡。

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