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. Author manuscript; available in PMC: 2009 Aug 1.
Published in final edited form as: Placenta. 2008 Jun 20;29(8):708–717. doi: 10.1016/j.placenta.2008.05.005

Fig 5. Role of ERK2/1, JNK1/2 and PI3K/AKT1 in FGF2 upregulation of eNOS in oFPAE cells.

Fig 5

Panels A, C and E - Pharmacological inhibition of FGF2-induced kinase activation: Cells were pretreated with increasing concentrations of the specific inhibitors PD98059 (MEK1/ERK2/1), SP600125 (JNK1/2) and Wortmannin (PI3K/AKT1) for 60 min, followed by treatment with 10 ng/ml FGF2 for 10 min. Protein samples were prepared for analyzing kinase phosphorylation as described in Fig. 2-4. Representative immunoblots (A, C and E) of one typical experiment show dose-dependent inhibition of ERK2/1, JNK1/2, and AKT1 by each inhibitor to block FGF2 induced phosphorylation of its corresponding kinase. Panels B, D, and F – Involvement of kinase pathways in FGF upregulation of eNOS protein: Serum-starved cells were pretreated with or without increasing concentrations of each inhibitor for 60 min, followed by treatment with or without 10 ng/ml FGF2 for 24 h. Bar graphs summarize data (Means ± SEM, n=3) of eNOS/β-actin protein levels relative to controls. Bars with different superscripts differ significantly (p<0.05).