Research Paper Volume 12, Issue 14 pp 14830—14848

FGF2-induced PI3K/Akt signaling evokes greater proliferation and adipogenic differentiation of human adipose stem cells from breast than from abdomen or thigh

Figure 6. Promotion of adipogenic differentiation by FGF2 via the PI3K/Akt signaling pathway in vitro. (A) Correlation analysis plot of the FGF2-PI3K/Akt signaling pathway. (B) Potential mechanism by which this pathway enhances proliferation and differentiation of hbASCs. (C) Oil Red O staining of hbASCs showing that FGF2 promoted adipogenic differentiation. (D) Oil Red O staining of htASCs showing that FGF2 promoted adipogenic differentiation. (E) Oil Red O staining of haASCs showing that FGF2 promoted adipogenic differentiation. Akt and PPARγ2 levels were significantly higher in group B than in groups A, C, or D, based on western blot. LY294002 suppressed adipogenic differentiation of htASCs, haASCs, and hbASCs based on Oil Red O staining, while down-regulating Akt and PPARγ2 based on western blotting. *P<0.01, **P<0.01. Group descriptions: (A) basic adipogenic induction medium (BM); (B) BM+FGF2 (0.1 μg/mL); (C) BM+LY294002; (D) BM+FGF2 (0.1 μg/mL)+LY294002. Magnification of panels A1-D1, 200×. Magnification of panels A2-D2, 400×.