NANOG Attenuates Hair Follicle-Derived Mesenchymal Stem Cell Senescence by Upregulating PBX1 and Activating AKT Signaling
Blocking p-AKT or AKT knockdown significantly downregulates PBX1; upregulates p16, p53, and p21; and enhances cell senescence. (a, b) HF-MSCs that were ectopically expressing NANOG were treated with the PI3K/AKT inhibitor LY294002 (40 μM, 24 h). Western blotting shows that after the inhibition of PI3K/AKT signaling, the expression of p16, p53, p21, PBX1, and p-AKT was significantly altered. (c) Senescence-associated β-galactosidase (SA-β-gal) staining was used to examine cellular senescence after inhibiting the PI3K/AKT pathway. Scale . (d, e) HF-MSCs that were ectopically expressing NANOG were treated with AKT shRNA. Western blotting shows that knocking down AKT resulted in the downregulation of PBX1 and an increase in the expression of p16 and p21. Differences in the expression of p16, p21, PBX1, AKT, and p-AKT were statistically significant. (f) SA-β-gal staining was used to examine cellular senescence after knocking down AKT. Scale . (,,).