The Age-Dependent Transcription Factor Snai2 Suppresses p53/p21-Dependent Cellular Senescence under VP-16-Induced DNA Damage

Studies on aging in the intestinal tract, which contributes to gut frailty, are limited.We aimed to screen proteins specifically expressed in the mouse intestinal tract during the neonatal period and to elucidate their functions.Murine adult fibroblast L929 cells and ICR mice were used for the study.Candidate proteins were screened by microarray analysis, and protein and mRNA expression were assessed by western blotting and reverse transcription-polymerase chain reaction, respectively.Moreover, cells and tissues from mice were subjected to histological analysis.Snai2 overexpression in adult-derived cells significantly suppressed senescence-associated β-galactosidase (SA-β-gal) activity under DNA damage conditions.Conversely, knockdown of Snai2 in fetus-derived cells exacerbated DNA damage-induced SA-β-gal activity and TRP53 expression, suggesting that SNAI2 functions to suppress cellular senescence in normal cells under DNA damage conditions. Materials and Methods CellsMurine adult fibroblast L929 cells were purchased from Japanese Collection of Research Bioresources (Osaka, Japan) AgingBio, 4, e20260045,