Fig. 5. Effect of PKC activation on the proliferative capacity of OPs on Vn. OPs were either left untreated (ctrl, PDGF, PMA) or were pre- exposed to PD098059 (PD, 50 µM), AG1295 (AG, 10 µM), wortmannin (WM, 50 nM) or BIM (0.5 µM) for 30 min at 37°C (in suspension), plated on Vn (10 µg/ml) and subsequently left untreated (ctrl) or treated with either 1 ng/ml PDGF (PDGF) or 100 nM PMA (all others, indicated by the horizontal bar), and the effect on proliferation was determined as described in Materials and methods. Values shown are means ± SD of at least three independent experiments, each in duplicate. Statistical significance is shown (***P <0.001) between PMA and the other indicated conditions. Note that PKC activation (in the absence of PDGF) via PMA mimicked the PDGF-mediated enhanced proliferation on Vn, and that inhibition of both PKC (BIM) and PI3K (WM) was able to abolish this enhanced proliferation.