Detalle Publicación

Systemic NF-kB-mediated inflammation promotes an aging phenotype in skeletal stem/progenitor cells
Autores: Josephson, A. M.; Leclerc, K.; Remark, L. H.; Muiños Lopez, Emma; Leucht, P. (Autor de correspondencia)
Título de la revista: AGING-US
ISSN: 1945-4589
Volumen: 13
Número: 10
Páginas: 13421 - 13429
Fecha de publicación: 2021
Aging tissues undergo a progressive decline in regenerative potential. This decline in regenerative responsiveness has been attributed to changes in tissue-specific stem cells and their niches. In bone, aged skeletal stem/progenitor cell dysfunction is characterized by decreased frequency and impaired osteogenic differentiation potential. This aging phenotype ultimately results in compromised regenerative responsiveness to injury. The age-associated increase of inflammatory mediators, known as inflamm-aging, has been identified as the main culprit driving skeletal stem cell dysfunction. Here, we utilized a mouse model of parabiosis to decouple aging from inflammation. Using the Nfkb1-/- mouse as a model of inflamm-aging, we demonstrate that a shared systemic circulation between a wild-type and Nfkb1-/- mouse results in an aging phenotype of the wild-type skeletal stem and progenitor cells, shown by CFUfs and osteogenic and adipogenic differentiation assays. Our findings demonstrate that exposure to an inflammatory secretome results in a phenotype similar to the one observed in aging.