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. Author manuscript; available in PMC: 2016 May 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2015 Mar 19;35(5):1147–1155. doi: 10.1161/ATVBAHA.114.304752

Figure 6.

Figure 6

β-catenin nuclear translocation is promoted by adrenomedullin and is dependent on GJIC. A. Treatment of LECs with 10nM human AM caused an alignment of β-catenin at the membrane along with its nuclear translocation. These changes were prevented by pretreatment with AM inhibitor AM22-52 (1µM). The gap junction inhibitor CBX (100µM) prevented β-catenin nuclear translocation indicating that GJIC is necessary for its translocation. Magnification: 40X. Scale bar: 50µm. B. Quantification showing the percentage of cells with β-catenin nuclear translocation relative to the total number of cells in the field. 80-120 cells were analyzed for each treatment from 3 independent experiments and expressed as means ± SE. C. RNA isolated from LECs treated with vehicle or 10nM human AM (4hrs) was analyzed by qPCR for expression of C-MYC. D. The model depicts how high tumor-derived AM promotes increased tumor cell adhesion to LECs, connexin-mediated GJIC, β-catenin nuclear translocation and subsequent gene transcription to facilitate transendothelial migration.