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首页> 外文期刊>American Journal of Physiology >Monocytic cell necrosis is mediated by potassium depletion and caspase-like proteases.
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Monocytic cell necrosis is mediated by potassium depletion and caspase-like proteases.

机译：单核细胞坏死是由钾耗竭和半胱天冬酶样蛋白酶介导的。

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摘要

Apoptosis is a physiological cell death that culminates in mitochondrial permeability transition and the activation of caspases, a family of cysteine proteases. Necrosis, in contrast, is a pathological cell death characterized by swelling of the cytoplasm and mitochondria and rapid plasma membrane disruption. Necrotic cell death has long been opposed to apoptosis, but it now appears that both pathways involve mitochondrial permeability transition, raising the question of what mediates necrotic cell death. In this study, we investigated mechanisms that promote necrosis induced by various stimuli (Clostridium difficile toxins, Staphylococcus aureus alpha toxin, ouabain, nigericin) in THP-1 cells, a human monocytic cell line, and in monocytes. All stimuli induced typical features of necrosis and triggered protease-mediated release of interleukin-1beta (IL-1beta) and CD14 in both cell types. K+ depletion was actively implicated in necrosis because substituting K+ for Na+ in the extracellular medium prevented morphological features of necrosis and IL-1beta release. N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone, a broad-spectrum caspase inhibitor, prevented morphological features of necrosis, plasma membrane destruction, loss of mitochondrial membrane potential, IL-1beta release, and CD14 shedding induced by all stimuli. Thus, in monocytic cells, necrosis is a cell death pathway mediated by passive K+ efflux and activation of caspase-like proteases.
机译：凋亡是一种生理细胞死亡，最终导致线粒体通透性转变和半胱氨酸蛋白酶家族半胱氨酸蛋白酶的激活。相反，坏死是一种病理性细胞死亡，其特征在于细胞质和线粒体肿胀以及快速的质膜破裂。坏死细胞的死亡长期以来一直与细胞凋亡相反，但是现在看来这两种途径都涉及线粒体通透性的转变，这提出了介导坏死细胞死亡的媒介的问题。在这项研究中，我们研究了在THP-1细胞，人单核细胞系和单核细胞中促进各种刺激（艰难梭菌毒素，金黄色葡萄球菌α毒素，哇巴因，尼日利亚菌素）引起的坏死的机制。在两种细胞类型中，所有刺激均诱导坏死的典型特征并触发蛋白酶介导的白介素-1β（IL-1beta）和CD14释放。 K +耗竭积极地参与了坏死，因为用K +代替细胞外培养基中的Na +可以防止坏死和IL-1β释放的形态学特征。 N-苄氧基羰基-Val-Ala-Asp-氟甲基酮，广谱半胱天冬酶抑制剂，可防止坏死的形态学特征，质膜破坏，线粒体膜电位丧失，IL-1beta释放和所有刺激物引起的CD14脱落。因此，在单核细胞中，坏死是由被动K +外排和半胱天冬酶样蛋白酶激活介导的细胞死亡途径。

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