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首页> 外文期刊>Molecular and Cellular Biology >Autophagy Is Activated for Cell Survival after Endoplasmic Reticulum Stress
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Autophagy Is Activated for Cell Survival after Endoplasmic Reticulum Stress

机译：自噬激活内质网应激后的细胞存活。

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Eukaryotic cells deal with accumulation of unfolded proteins in the endoplasmic reticulum (ER) by the unfolded protein response, involving the induction of molecular chaperones, translational attenuation, and ER-associated degradation, to prevent cell death. Here, we found that the autophagy system is activated as a novel signaling pathway in response to ER stress. Treatment of SK-N-SH neuroblastoma cells with ER stressors markedly induced the formation of autophagosomes, which were recognized at the ultrastructural level. The formation of green fluorescent protein (GFP)-LC3-labeled structures (GFP-LC3“ dots”), representing autophagosomes, was extensively induced in cells exposed to ER stress with conversion from LC3-I to LC3-II. In IRE1-deficient cells or cells treated with c-Jun N-terminal kinase (JNK) inhibitor, the autophagy induced by ER stress was inhibited, indicating that the IRE1-JNK pathway is required for autophagy activation after ER stress. In contrast, PERK-deficient cells and ATF6 knockdown cells showed that autophagy was induced after ER stress in a manner similar to the wild-type cells. Disturbance of autophagy rendered cells vulnerable to ER stress, suggesting that autophagy plays important roles in cell survival after ER stress.
机译：真核细胞通过未折叠的蛋白质反应处理未折叠蛋白质在内质网（ER）中的积累，涉及诱导分子伴侣，翻译减弱和与ER相关的降解，以防止细胞死亡。在这里，我们发现自噬系统被激活为响应内质网应激的新型信号通路。用ER应激源处理SK-N-SH神经母细胞瘤细胞可明显诱导自噬体的形成，这在超微结构水平已得到认可。代表自噬体的绿色荧光蛋白（GFP）-LC3标记的结构（GFP-LC3“点”）的形成在暴露于内质网应激的细胞中被广泛诱导，并从LC3-I转化为LC3-II。在IRE1缺陷细胞或经c-Jun N末端激酶（JNK）抑制剂处理的细胞中，内质网应激诱导的自噬被抑制，这表明内质网应激后自噬激活需要IRE1-JNK途径。相比之下，PERK缺陷细胞和ATF6敲低细胞表明内质网应激后以与野生型细胞相似的方式诱导自噬。自噬的干扰使细胞易受内质网应激的影响，表明自噬在内质网应激后的细胞存活中起重要作用。

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