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. 2015 Sep 28;2(11):1767–1784. doi: 10.1016/j.ebiom.2015.09.042

Fig. 8.

Fig. 8

p38MAPKβ mediates VEGFC-induced angiogenic events. A. An equal amount of protein from control and various time periods of VEGFC (100 ng/ml)-treated HRMVECs were analyzed by Western blotting for pJNK1 and pp38MAPK levels using their phospho-specific antibodies and normalized to their total levels. B. Cells were transduced with Ad-GFP, Ad-JNK1 or Ad-dnp38MAPKβ (p38β) (40 moi), growth-arrested, treated with and without VEGFC (100 ng/ml) for 10 min and cell extracts were prepared and analyzed for pCREB levels using its phospho-specific antibodies and the blot was sequentially reprobed for CREB, JNK1, p38MAPK and β-tubulin levels to show the over expression of dnJNK1, dnp38β or normalization. C. Cells were transduced with Ad-GFP or Ad-dnp38β (40 moi), growth-arrested, treated with and without VEGFC (100 ng/ml) for 2 h and cell extracts were prepared and analyzed for DLL4 or cNOTCH1 levels using their specific antibodies and the blot was sequentially reprobed for p38β and β-tubulin to show the over expression of dnp38β or normalization. D–G. Cells were transduced with Ad-GFP or Ad-dnp38β (40 moi), growth-arrested and subjected to DNA synthesis (D), migration (E), tube formation (F) or sprouting assay (G). The bar graphs represent quantitative analysis of 3 independent experiments. The values are presented as Mean ± SD. * p < 0.01 vs control; ** p < 0.01 vs control siRNA + VEGFC. Scale bar represents 50 μm in panel E.