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溶酶体靶向剂,包括阿奇霉素、氯喹和羟氯喹,激活整合应激反应。

Lysosomotropic agents including azithromycin, chloroquine and hydroxychloroquine activate the integrated stress response.

机构信息

Centre de Recherche des Cordeliers, Equipe labellisée par la Ligue contre le cancer, Université de Paris, Sorbonne Université, Inserm U1138, Institut Universitaire de France, Paris, France.

Metabolomics and Cell Biology Platforms, Gustave Roussy, Villejuif, France.

出版信息

Cell Death Dis. 2021 Jan 6;12(1):6. doi: 10.1038/s41419-020-03324-w.

Abstract

The integrated stress response manifests with the phosphorylation of eukaryotic initiation factor 2α (eIF2α) on serine residue 51 and plays a major role in the adaptation of cells to endoplasmic reticulum stress in the initiation of autophagy and in the ignition of immune responses. Here, we report that lysosomotropic agents, including azithromycin, chloroquine, and hydroxychloroquine, can trigger eIF2α phosphorylation in vitro (in cultured human cells) and, as validated for hydroxychloroquine, in vivo (in mice). Cells bearing a non-phosphorylatable eIF2α mutant (S51A) failed to accumulate autophagic puncta in response to azithromycin, chloroquine, and hydroxychloroquine. Conversely, two inhibitors of eIF2α dephosphorylation, nelfinavir and salubrinal, enhanced the induction of such autophagic puncta. Altogether, these results point to the unexpected capacity of azithromycin, chloroquine, and hydroxychloroquine to elicit the integrated stress response.

摘要

整合应激反应表现为真核起始因子 2α(eIF2α)丝氨酸 51 位的磷酸化,在细胞对内质网应激的适应中发挥主要作用,可启动自噬和引发免疫反应。在这里,我们报告说溶酶体增敏剂,包括阿奇霉素、氯喹和羟氯喹,可在体外(在培养的人细胞中)和体内(在小鼠中,经羟氯喹验证)触发 eIF2α 的磷酸化。对阿奇霉素、氯喹和羟氯喹不发生磷酸化的 eIF2α 突变体(S51A)的细胞不能积累自噬斑点。相反,两种 eIF2α 去磷酸化抑制剂,奈非那韦和 salubrinal,增强了这种自噬斑点的诱导。总的来说,这些结果表明阿奇霉素、氯喹和羟氯喹具有出人意料的引发整合应激反应的能力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1141/7790833/7c6059b95974/41419_2020_3324_Fig1_HTML.jpg

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