DOUSSET, Lea; MAHFOUF, Walid; YOUNES, Hadi; FATROUNI, Hala; FAUCHEUX, Corinne; MUZOTTE, Elodie; KHALIFE, Ferial; ROSSIGNOL, Rodrigue; MOISAN, Francois; CARIO, Muriel; CLAVEROL, Stéphane; FAVOT-LAFORGE, Laure; NIEMINEN, Anni I; VAINIO, Seppo; ALI, Nsrein; REZVANI, Hamid Reza

doi:10.1016/j.freeradbiomed.2024.12.030

BoRdeaux Institute in onCology [Inserm U1312 - BRIC]

MAHFOUF, Walid
BoRdeaux Institute in onCology [Inserm U1312 - BRIC]

YOUNES, Hadi
BoRdeaux Institute in onCology [Inserm U1312 - BRIC]

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Free Radical Biology and Medicine. 2024-12-10, vol. 227, p. 459-471

Résumé en anglais

Solar ultraviolet B (UVB) radiation-induced DNA damage is a well-known initiator of skin carcinomas. The UVB-induced DNA damage response (DDR) involves series of signaling cascades that are activated to maintain cell integrity. Among the different biological processes, little is known about the role of energy metabolism in the DDR. We sought to determine whether UVB-induced nuclear and/or mitochondrial cyclobutane pyrimidine dimers (CPDs) alter cellular energy metabolism. To gain insight into this question, we took advantage of keratinocytes expressing nuclear or mitochondrial CPD photolyase. Applying a quantitative proteomic approach and targeted metabolomics, we observed biphasic alterations in multiple metabolic pathways and in the abundance of various metabolites, largely influenced by the presence of genomic CPDs. The heightened oxygen consumption rate post-irradiation, along with mitochondrial structural rearrangements, was found to be dependent on both mitochondrial and nuclear CPDs. Understanding the influence of nuclear and mitochondrial DNA damage on keratinocyte responses to UVB irradiation deepens current knowledge regarding skin cancer prevention, initiation, and therapy.< Réduire

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https://oskar-bordeaux.fr/handle/20.500.12278/204620

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http://dx.doi.org/10.1016/j.freeradbiomed.2024.12.030

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Maladies Rares : Génétique et Métabolisme (MRGM) - UMR 1211

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Energy metabolism rewiring following acute UVB irradiation is largely dependent on nuclear DNA damage.

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