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首页> 外文期刊>Cellular Physiology and Biochemistry >PGE(2)-induced apoptotic cell death in k562 human leukaemia cells
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PGE(2)-induced apoptotic cell death in k562 human leukaemia cells

机译：PGE（2）诱导k562人白血病细胞凋亡

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摘要

Prostaglandin-E-2 (PGE(2)) is known to trigger suicidal death of nucleated cells (apoptosis) and enucleated erythrocytes (eryptosis). In erythrocytes PGE(2) induced suicidal cell death involves activation of nonselective cation channels leading to Ca2+ entry followed by cell shrinkage and triggering of Ca2+ sensitive cell membrane scrambling with phosphatidylserine (PS) exposure at the cell surface. The present study was performed to explore whether PGE(2) induces apoptosis of nucleated cells similarly through cation channel activation and to possibly disclose the molecular identity of the cation channels involved. To this end, Ca2+ activity was estimated from Fluo3 fluorescence, mitochondrial potential from DePsipher fluorescence, phosphatidylserine exposure from annexin binding, caspase activation from caspAce fluorescence, cell volume from FACS forward scatter, and DNA fragmentation utilizing a photometric enzyme immunoassay. Stimulation of K562 human leukaemia cells with PGE(2) (50 mu M) increased cytosolic Ca2+ activity, decreased forward scatter, depolarized the mitochondrial potential, increased annexin binding, led to caspase activation and resulted in DNA fragmentation. Gene silencing of the Ca2+-permeable transient receptor potential cation channel TRPC7 significantly blunted PGE(2)-induced triggering of PS exposure and DNA fragmentation. In conclusion, K562 cells express Ca2+-permeable TRPC7 channels, which are activated by PGE(2) and participate in the triggering of apoptosis. Copyright (c) 2006 S. Karger AG, Basel.
机译：已知前列腺素-E-2（PGE（2））触发有核细胞和去核红细胞的自杀死亡（凋亡）。在红细胞中，PGE（2）诱导的自杀性细胞死亡涉及激活非选择性阳离子通道，导致Ca2 +进入，随后细胞收缩，并触发Ca2 +敏感细胞膜，在细胞表面暴露有磷脂酰丝氨酸（PS）。进行本研究以探讨PGE（2）是否通过阳离子通道激活类似地诱导有核细胞凋亡，并可能揭示所涉及阳离子通道的分子身份。为此，从Fluo3荧光，从DePsipher荧光得到的线粒体电位，从膜联蛋白结合得到的磷脂酰丝氨酸暴露，从caspAce荧光得到的胱天蛋白酶激活，从FACS向前散射得到的细胞体积以及利用光度酶免疫测定法的DNA断裂来估计Ca2 +活性。用PGE（2）（50μM）刺激K562人白血病细胞增加了胞质Ca2 +活性，减少了前向散射，使线粒体电位去极化，增加了膜联蛋白结合，导致胱天蛋白酶激活，并导致DNA断裂。 Ca2 +渗透性瞬时受体潜在阳离子通道TRPC7的基因沉默大大使PGE（2）诱导的PS暴露和DNA片段化触发。总之，K562细胞表达可透过Ca2 +的TRPC7通道，该通道被PGE（2）激活并参与细胞凋亡的触发。版权所有（c）2006 S.Karger AG，巴塞尔。

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