Overexpression of CERKL Protects Retinal Pigment Epithelium Mitochondria from Oxidative Stress Effects.

ABSTRACT: The precise function of CERKL, a Retinitis Pigmentosa (RP) causative gene, is not yet fully understood. There is evidence that CERKL is involved in the regulation of autophagy, stress granules, and mitochondrial metabolism, and it is considered a gene that is resilient against oxidative stress in the retina. Mutations in most RP genes affect photoreceptors, but retinal pigment epithelium (RPE) cells may be also altered. Here, we aimed to analyze the effect of CERKL overexpression and depletion in vivo and in vitro, focusing on the state of the mitochondrial network under oxidative stress conditions. Our work indicates that the depletion of CERKL increases the vulnerability of RPE mitochondria, which show a shorter size and altered shape, particularly upon sodium arsenite treatment. CERKL-d

SUBMITTER: Garcia-Arroyo R 

PROVIDER: S-EPMC8698444 | biostudies-literature | 2021 Dec

REPOSITORIES: biostudies-literature