SRA

Aging is marked by a progressive decline in physiological function, leading to an increased susceptibility to age-related diseases and cancer. On the cellular level, aging correlates with an accumulation of senescent cells, which play a dual role: they are critical for tissue homeostasis, yet their over-accumulation may drive pathological aging. We recently revealed that senescent cells could overexpress immunosuppressive molecules like the ganglioside GD3 at their cell surface to evade from immune surveillance and to facilitate their tolerogenicity. We investigate which cells expressed GD3 and whether this ganglioside could be considered as a new marker associated to senescence in a model of senescence associated disease: Bleomycin-induced lung fibrosis. Overall design: To characterize GD3 positive cells we induced lung fibrosis in young C57Bl6/J male mice by Bleomycin instillation. After 27 days, we collected the lungs, dissociated them and labeled them for GD3 as well as a know senescence marker: SA-ß-Gal. We then sorted the different fractions.