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Article

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

1
Department of Genetics, Microbiology and Statistics, Avda. Diagonal 643, Universitat de Barcelona, 08028 Barcelona, Spain
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CIBERER, Instituto de Salud Carlos III, 28029 Madrid, Spain
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Institut de Biomedicina-Institut de Recerca Sant Joan de Déu (IBUB-IRSJD), Universitat de Barcelona, 08028 Barcelona, Spain
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Department of Biochemistry and Molecular Biomedicine, Avda. Diagonal 643, Universitat de Barcelona, 08028 Barcelona, Spain
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CIBEROBN, Instituto de Salud Carlos III, 28029 Madrid, Spain
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DBGen Ocular Genomics, 08028 Barcelona, Spain
*
Authors to whom correspondence should be addressed.
Academic Editor: Isabel Pinilla
Antioxidants 2021, 10(12), 2018; https://doi.org/10.3390/antiox10122018
Received: 30 November 2021 / Revised: 14 December 2021 / Accepted: 17 December 2021 / Published: 19 December 2021
(This article belongs to the Special Issue Oxidative Stress in the Retina Diseases)
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-depleted cells have dysfunctional mitochondrial respiration particularly upon oxidative stress conditions. The overexpression of two human CERKL isoforms (558 aa and 419 aa), which display different protein domains, shows that a pool of CERKL localizes at mitochondria in RPE cells and that CERKL protects the mitochondrial network—both in size and shape—against oxidative stress. Our results support CERKL being a resilient gene that regulates the mitochondrial network in RPE as in retinal neurons and suggest that RPE cell alteration contributes to particular phenotypic traits in patients carrying CERKL mutations. View Full-Text
Keywords: retinitis pigmentosa; CERKL; retinal pigment epithelium; mitochondrial network; oxidative stress retinitis pigmentosa; CERKL; retinal pigment epithelium; mitochondrial network; oxidative stress
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MDPI and ACS Style

García-Arroyo, R.; Gavaldà-Navarro, A.; Villarroya, F.; Marfany, G.; Mirra, S. Overexpression of CERKL Protects Retinal Pigment Epithelium Mitochondria from Oxidative Stress Effects. Antioxidants 2021, 10, 2018. https://doi.org/10.3390/antiox10122018

AMA Style

García-Arroyo R, Gavaldà-Navarro A, Villarroya F, Marfany G, Mirra S. Overexpression of CERKL Protects Retinal Pigment Epithelium Mitochondria from Oxidative Stress Effects. Antioxidants. 2021; 10(12):2018. https://doi.org/10.3390/antiox10122018

Chicago/Turabian Style

García-Arroyo, Rocío, Aleix Gavaldà-Navarro, Francesc Villarroya, Gemma Marfany, and Serena Mirra. 2021. "Overexpression of CERKL Protects Retinal Pigment Epithelium Mitochondria from Oxidative Stress Effects" Antioxidants 10, no. 12: 2018. https://doi.org/10.3390/antiox10122018

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