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首页> 外文期刊>Cellular Physiology and Biochemistry >Inhibition of CD95/Fas-induced DNA degradation by osmotic cell shrinkage
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Inhibition of CD95/Fas-induced DNA degradation by osmotic cell shrinkage

机译：渗透细胞收缩抑制CD95 / Fas诱导的DNA降解

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Apoptosis (programmed cell death) is an active physiological mechanism from which removal of abundant or potentially harmful cells follows. Apoptosis of lymphocytes is critical for the development of the immune system and during the immune response. As we have shown previously, moderate osmotic cell shrinkage interferes with CD95 (Fas/Apo-1)-induced cell death. The present study has been performed to further elucidate the underlying mechanisms. To this end, apoptosis in Jurkat T-lymphocytes was elicited by triggering the CD95-receptor with monoclonal CD95/ Fas-antibody. Osmotic cell shrinkage which was induced by the addition of 100 mM NaCl, did not significantly interfere with CD95-induced phosphatidylserine exposure nor the activation of caspase 3 activity as determined by PARP cleavage, DEVD-AMC consumption, or the activation of PAK2-kinase. However, osmotic cell shrinkage almost abolished CD95-induced DNA fragmentation (as revealed by propidium iodide staining) and the activation of a DNase as evidenced from SDS-PAGE gel assay. Western blot analysis showed CD95-induced tyrosine phosphorylation of a nuclear protein of ca. 20 kD which comigrated with nuclease activity. This tyrosine phosphorylation was almost completely abolished by the addition of 100 mM NaCl. Furthermore, osmotic cell shrinkage blunted the CD95-induced activation of the Src-like kinase p56lck. It is concluded that different signaling pathways mediate FITC-Annexin-V binding and DNase activation. Only the latter is sensitive to osmotic cell shrinkage. Copyright (C) 2000 S. Karger AG, Basel. [References: 39]
机译：凋亡（程序性细胞死亡）是一种活跃的生理机制，可从中去除大量或潜在有害的细胞。淋巴细胞的凋亡对于免疫系统的发育和免疫反应至关重要。如我们先前所示，中等渗透性细胞收缩会干扰CD95（Fas / Apo-1）诱导的细胞死亡。进行本研究是为了进一步阐明潜在的机制。为此，通过用单克隆CD95 / Fas抗体触发CD95受体来引发Jurkat T淋巴细胞的凋亡。通过添加100 mM NaCl诱导的渗透性细胞收缩不会显着干扰CD95诱导的磷脂酰丝氨酸暴露，也不会干扰caspase 3活性的活化（通过PARP裂解，DEVD-AMC消耗或PAK2-激酶的活化来确定）。然而，渗透细胞的收缩几乎消除了CD95诱导的DNA片段化（如碘化丙啶染色所揭示的）和DNase的活化，如SDS-PAGE凝胶分析所证明的。蛋白质印迹分析显示CD95诱导的酪氨酸磷酸化约一个核蛋白。与核酸酶活性有关的20kD。添加100 mM NaCl几乎完全消除了酪氨酸磷酸化。此外，渗透细胞的收缩使CD95诱导的Src样激酶p56lck的激活减弱。结论是不同的信号通路介导FITC-Annexin-V结合和DNase激活。只有后者对渗透细胞收缩敏感。版权所有（C）2000 S.Karger AG，巴塞尔。 [参考：39]

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