Skip to main content
. Author manuscript; available in PMC: 2020 Apr 1.
Published in final edited form as: Matrix Biol. 2018 Sep 4;77:101–116. doi: 10.1016/j.matbio.2018.08.010

Figure 4. FGF10- or GDNF-induced cellular spreading and proliferation mediated by LM-binding integrins is regulated by Akt.

Figure 4.

Itgα3f/fα6f/f CD cells were treated with DMSO or Akt inhibitor IV (5 μM) for 1 h, plated on LM-511 for 1 h and then treated with or without FGF10 (A) or GDNF (B) (10 ng/ml each). Cell spreading (A-B) and proliferation (C) were evaluated at 1 and 24 h after addition of growth factors, respectively. (A) Representative confocal images of the cells stained with rhodamine-phalloidin are shown; bar: 10 μM. (B) The individual measurements of cell surface (in pixels) of 15-30 cells with the mean is shown; *p≤0.05 between Itgα3f/fα6f/f CD cells pretreated with DMSO and Akt Inh. IV. ≤0.05 between Itgα3f/fα6f/f untreated or treated with FGF10 or GDNF. (C) Proliferation as measured by the OD of BrdU-positive cells ±SEM of 4-6 independent experiments is shown; *p≤0.05 between cells treated with DMSO and Akt Inh.IV. ≤0.05 between Itgα3f/fα6f/f untreated or treated with FGF10 or GDNF. (D-E) Phosphorylation of Akt was evaluated 5, 15 and 30 min after addition of FGF10 (D) or GDNF (E). β-actin was used as loading control.