Please use this identifier to cite or link to this item:http://hdl.handle.net/20.500.12105/7531
Polμ deficiency increases resistance to oxidative damage and delays liver aging
Escudero, Beatriz CNIC | Lucas, Daniel | Albo-Castellanos, Carmen CNIC | Dhup, Suveera CNIC | Bacher, Jeff W | Sánchez-Muñoz, Aránzazu | Fernández, Margarita | Rivera-Torres, Jose CNIC | Carmona, Rosa M CNIC | Fuster, Encarnación | Carreiro, Candelas CNIC | Bernad, Raquel | Gonzalez, Manuel A CNIC | Andres, Vicente CNIC | Blanco, Luis | Roche, Enrique | Fabregat, Isabel | Samper, Enrique CNIC | Bernad, Antonio CNIC
PLoS One. 2014; 9(4):e93074
Polμ is an error-prone PolX polymerase that contributes to classical NHEJ DNA repair. Mice lacking Polμ (Polμ(-/-)) show altered hematopoiesis homeostasis and DSB repair and a more pronounced nucleolytic resection of some V(D)J junctions. We previously showed that Polμ(-/-) mice have increased learning capacity at old ages, suggesting delayed brain aging. Here we investigated the effect of Polμ(-/-) deficiency on liver aging. We found that old Polμ(-/-) mice (>20 month) have greater liver regenerative capacity compared with wt animals. Old Polμ(-/-) liver showed reduced genomic instability and increased apoptosis resistance. However, Polμ(-/-) mice did not show an extended life span and other organs (e.g., heart) aged normally. Our results suggest that Polμ deficiency activates transcriptional networks that reduce constitutive apoptosis, leading to enhanced liver repair at old age.
Aging | Animals | DNA-Directed DNA Polymerase | Genomic Instability | Liver | Liver Function Tests | Mice, Inbred BALB C | Mice, Inbred C57BL | Models, Biological | Myocardium | Phenotype | Sister Chromatid Exchange | Oxidative Stress
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