| Literature DB >> 33414432 |
Ai-Ling Tian1,2, Qi Wu1,2,3, Peng Liu1,2, Liwei Zhao1,2, Isabelle Martins1,2, Oliver Kepp4,5, Marion Leduc1,2, Guido Kroemer6,7,8,9,10.
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.Entities:
Year: 2021 PMID: 33414432 PMCID: PMC7790317 DOI: 10.1038/s41419-020-03324-w
Source DB: PubMed Journal: Cell Death Dis Impact factor: 8.469