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首页> 外文期刊>Journal of cellular biochemistry. >Vacuolar H+ -ATPase c protects glial cell death induced by sodium nitroprusside under glutathione-depleted condition.
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Vacuolar H+ -ATPase c protects glial cell death induced by sodium nitroprusside under glutathione-depleted condition.

机译：在谷胱甘肽缺乏的条件下，液泡H + -ATPase c保护由硝普钠引起的神经胶质细胞死亡。

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摘要

We examined the role of the c subunit (ATP6L) of vacuolar H(+) -ATPase and its molecular mechanisms in glial cell death induced by sodium nitroprusside (SNP). ATP6L siRNA-transfected cells treated with SNP showed a significant increase in cytotoxicity under glutathione (GSH)-depleted conditions after pretreatment with buthionine sulfoximine, but reduction of ATP6L did not affect the regulation of lysosomal pH in analyses with lysosomal pH-dependent fluorescence probes. Photodegraded SNP and ferrous sulfate induced cytotoxicity with the same pattern as that of SNP, but SNAP and potassium cyanide did not show activity. Pretreatment of the transfected cells with deferoxamine (DFO) reduced ROS production and significantly inhibited the cytotoxicity, which indicates that primarily iron rather than nitric oxide or cyanide from SNP contributes to cell death. Involvement of apoptotic processes in the cells was not shown. Pretreatment with JNK or p38 chemical inhibitor significantly inhibited the cytotoxicity, and we also confirmed that the MAPKs were activated in the cells by immunoblot analysis. Significant increase of LC3-II conversion was observed in the cells, and the conversions were inhibited by cotransfection of the MAPK siRNAs and pretreatment with DFO. Introduction of Atg5 siRNA inhibited the cytotoxicity and inhibited the activation of MAPKs and the conversion of LC3. We finally confirmed autophagic cell death and involvement of MAPKs by observation of autophagic vacuoles via electron microscopy. These data suggest that ATP6L has a protective role against SNP-induced autophagic cell death via inhibition of JNK and p38 in GSH-depleted glial cells.
机译：我们检查了液泡H（+）-ATPase的c亚基（ATP6L）的作用及其分子机制在硝普钠（SNP）诱导的神经胶质细胞死亡中。经SNP处理的ATP6L siRNA转染的细胞在用丁硫氨酸亚砜亚胺预处理后，在谷胱甘肽（GSH）耗尽的条件下显示出细胞毒性的显着增加，但在溶酶体pH依赖性荧光探针分析中，ATP6L的降低并不影响溶酶体pH的调节。光降解的SNP和硫酸亚铁以与SNP相同的模式诱导细胞毒性，但是SNAP和氰化钾没有显示活性。用去铁胺（DFO）预处理转染的细胞可减少ROS的产生并显着抑制细胞毒性，这表明主要是铁而不是SNP的一氧化氮或氰化物会导致细胞死亡。没有显示细胞中凋亡过程的参与。用JNK或p38化学抑制剂预处理可显着抑制细胞毒性，并且我们还通过免疫印迹分析证实了MAPK在细胞中被激活。在细胞中观察到LC3-II转化的显着增加，并且通过MAPK siRNA的共转染和DFO预处理抑制了转化。 Atg5 siRNA的导入可抑制细胞毒性，并抑制MAPKs的活化和LC3的转化。通过电子显微镜观察自噬泡，我们最终证实了自噬细胞的死亡和MAPK的参与。这些数据表明，ATP6L通过抑制GSH缺失的神经胶质细胞中的JNK和p38，对SNP诱导的自噬细胞死亡具有保护作用。

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