Delayed effects of radiation in adipose tissue reflect progenitor damage and not cellular senescence.

ABSTRACT: The pathogenesis of many age-related diseases is linked to cellular senescence, a state of inflammation-inducing, irreversible cell cycle arrest. The consequences and mechanisms of age-associated cellular senescence are often studied using in vivo models of radiation exposure. However, it is unknown whether radiation induces persistent senescence, like that observed in ageing. We performed analogous studies in mice and monkeys, where young mice and rhesus macaques received sub-lethal doses of ionizing radiation and were observed for ~ 15% of their expected lifespan. Assessments of 8-hydroxy-2' -deoxyguanosine (8-OHdG), senescence-associated beta-galactosidase (SAβ-gal), and p16^Ink4a and p21 were performed on mitotic and post-mitotic tissues - liver and adipose tissue - 6 months

SUBMITTER: Ruggiero AD 

PROVIDER: S-EPMC9886706 | biostudies-literature | 2023 Feb

REPOSITORIES: biostudies-literature