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首页> 外文期刊>Journal of Cellular Physiology >Calpain and calpastatin regulate neutrophil apoptosis.
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Calpain and calpastatin regulate neutrophil apoptosis.

机译：Calpain和calpastatin调节中性粒细胞细胞凋亡。

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摘要

The average polymorphonuclear neutrophil (PMN) lives only a day and then dies by apoptosis. We previously found that the calcium-dependent protease calpain is required for apoptosis in several mouse models of cell death. Here we identify calpain, and its endogenous inhibitor calpastatin, as regulators of human neutrophil apoptosis. Cell death triggered by the translation inhibitor cycloheximide is calpain-dependent, as evidenced using either a calpain active site inhibitor (N-acetyl-leucyl-leucyl-norleucinal) or agents that target calpain's calcium binding sites (PD150606, PD151746). No significant effect on cycloheximide-triggered apoptosis was found by using inhibitors of the proteasome or of other papain-like cysteine proteases, providing further evidence that the active site calpain inhibitor prevents apoptosis via its action on calpain. In addition, we find that potentiation of calpain activity by depleting its endogenous inhibitor, calpastatin, is sufficient to cause apoptosis of neutrophils. Nevertheless, apoptosis signalled via the Fas antigen proceeds regardless of the presence of calpain inhibitor. These experiments support a growing body of work, indicating an upstream regulatory role for calpain in many, but not all, forms of apoptotic cell death. They also identify calpastatin as a participant in apoptotic cell death and suggest that for at least one cell type, a decrease in calpastatin is a sufficient stimulus to initiate calpain-dependent apoptosis.
机译：平均多形核中性粒细胞(中性粒细胞)生命只有一天,然后死去的细胞凋亡。之前发现calcium-dependent蛋白酶calpain需要细胞凋亡一些细胞死亡的小鼠模型。识别calpain,其内源性抑制剂calpastatin,人类嗜中性粒细胞的监管机构细胞凋亡。翻译抑制剂环己酰亚胺使用一个calpain-dependent,就是明证calpain活性位点抑制剂(N-acetyl-leucyl-leucyl-norleucinal)或代理这一目标calpain的钙结合位点(PD150606 PD151746)。cycloheximide-triggered凋亡被发现使用的蛋白酶体抑制剂或其他papain-like半胱氨酸蛋白酶,进一步提供证据表明,活性部位calpain抑制剂防止细胞凋亡calpain通过其行动。此外,我们发现calpain的强化活动通过耗尽其内源性抑制剂,calpastatin,足以引起的细胞凋亡中性粒细胞。通过Fas抗原收益不管calpain抑制剂的存在。支持越来越多的工作,表示一个上游的监管角色calpain在很多,但是不是全部,凋亡细胞死亡形式。识别calpastatin参与凋亡细胞死亡和建议至少一个细胞类型,calpastatin减少足够的刺激来启动calpain-dependent细胞凋亡。

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