Optineurin modulates ER stress-induced signaling pathways and cell death.

Gopalakrishna Ramachandran, Shivranjani C Moharir, Tirumalai R Raghunand, Ghanshyam Swarup

Biochemical and biophysical research communications 2021 Jan 01

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We have investigated the physiological role of the autophagy receptor Optineurin/Optn in endoplasmic reticulum (ER) stress response using cellular and animal models. In comparison to their normal counterparts, Optn-deficient mouse embryonic fibroblasts showed significantly higher cell death and caspase-3 activation upon treatment with tunicamycin and thapsigargin, inducers of ER stress. The transcript levels of some of the genes regulated by the IRE1-XBP1 and PERK-ATF4 pathways were upregulated in Optn-deficient cells, in comparison with normal cells, upon treatment with tunicamycin, and also in the brain cortex and liver of tunicamycin treated Optn-deficient mice. Also, the basal levels of IRE1α and PERK were higher in Optn-deficient cells. These results suggest that Optn modulates ER stress-induced signaling pathways and provides protection from ER stress-induced cell death. Copyright © 2020 Elsevier Inc. All rights reserved.

Citation

Gopalakrishna Ramachandran, Shivranjani C Moharir, Tirumalai R Raghunand, Ghanshyam Swarup. Optineurin modulates ER stress-induced signaling pathways and cell death. Biochemical and biophysical research communications. 2021 Jan 01;534:297-302