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首页> 外文期刊>Molecular and Cellular Biology >Loss of Mcl-1 Protein and Inhibition of Electron Transport Chain Together Induce Anoxic Cell Death
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Loss of Mcl-1 Protein and Inhibition of Electron Transport Chain Together Induce Anoxic Cell Death

机译：Mcl-1蛋白的丢失和电子传输链的抑制共同导致缺氧性细胞死亡

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How cells die in the absence of oxygen (anoxia) is not understood. Here we report that cells deficient in Bax and Bak or caspase-9 do not undergo anoxia-induced cell death. However, the caspase-9 null cells do not survive reoxygenation due to the generation of mitochondrial reactive oxygen species. The individual loss of Bim, Bid, Puma, Noxa, Bad, caspase-2, or hypoxia-inducible factor 1β, which are potential upstream regulators of Bax or Bak, did not prevent anoxia-induced cell death. Anoxia triggered the loss of the Mcl-1 protein upstream of Bax/Bak activation. Cells containing a mitochondrial DNA cytochrome b 4-base-pair deletion ([rho?] cells) and cells depleted of their entire mitochondrial DNA ([rho0] cells) are oxidative phosphorylation incompetent and displayed loss of the Mcl-1 protein under anoxia. [rho0] cells, in contrast to [rho?] cells, did not die under anoxia. However, [rho0] cells did undergo cell death in the presence of the Bad BH3 peptide, an inhibitor of Bcl-XL/Bcl-2 proteins. These results indicate that [rho0] cells survive under anoxia despite the loss of Mcl-1 protein due to residual prosurvival activity of the Bcl-XL/Bcl-2 proteins. Collectively, these results demonstrate that anoxia-induced cell death requires the loss of Mcl-1 protein and inhibition of the electron transport chain to negate Bcl-XL/Bcl-2 proteins.
机译：在没有氧气（缺氧）的情况下细胞如何死亡尚不清楚。在这里我们报告缺乏Bax和Bak或caspase-9的细胞不会经历缺氧诱导的细胞死亡。但是，由于线粒体活性氧的产生，caspase-9空细胞不能在复氧中存活。 Bim，Bid，Puma，Noxa，Bad，caspase-2或缺氧诱导因子1β的个体丧失（可能是Bax或Bak的上游调节因子）不能阻止缺氧诱导的细胞死亡。缺氧触发了Bax / Bak激活上游Mcl-1蛋白的丢失。含有线粒体DNA细胞色素 b 4个碱基对缺失的细胞（[ rho ？]细胞）和耗尽了整个线粒体DNA的细胞（ [ rho 0 ]细胞）不能进行氧化磷酸化，并且在缺氧条件下显示Mcl-1蛋白的丢失。与[ rho ？]细胞相比，[ rho 0 ]细胞在缺氧下并未死亡。但是，[ rho 0 ]细胞确实在Bad BH3肽（Bcl-X L / Bcl的抑制剂）存在下经历了细胞死亡。 -2蛋白。这些结果表明，[ rho 0 ]细胞在缺氧条件下仍能存活，尽管由于Bcl-X L的残余存活活性导致Mcl-1蛋白丢失。 sub> / Bcl-2蛋白。总的来说，这些结果表明缺氧诱导的细胞死亡需要Mcl-1蛋白的丢失和电子传输链的抑制以否定Bcl-X L / Bcl-2蛋白。

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