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

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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×.