PKA promotes VE-cadherin–mediated endothelial cell-cell adhesion. (A) Endothelial cell tube formation in Matrigel was measured in the presence of culture medium (untreated), culture medium plus vehicle control (DMSO), or culture medium plus forskolin. Brightfield and fluorescence (4′,6-diamidino-2-phenylindole) images of Matrigel cultures are shown. (B) Quantification of vessel-like branchpoints per 100× microscopic field ± SEM formed by the network of tubes in each treatment condition, *P = .0001. (C) Quantification of cell number per branchpoint ± SEM in each treatment condition, *P = .005. (D) VE-cadherin immunostaining (green) of N1-GFP, pcDNA3.1V5/His dnPKA, and pcDNA3.1V5/His PKACat transfected endothelial cells in the absence (−forskolin) or presence of 20 μg/mL forskolin (+forskolin). (E) Percent adherent cells ± SEM in cells from D, *P < .05. Inset: Western blotting of transfected cells for expression of His-tagged PKA transgenes. (F) Top images: endothelial cell tube formation in Matrigel cultures in the presence of vehicle control (DMSO), forskolin, and PTHrP. Bottom images: VE-cadherin cell-cell contact formation in the presence of DMSO, forskolin, or PTHrP. (G) Cell number/branchpoint in DMSO, forskolin, or PTHrP-treated Matrigel cultures. (H) Percent adherent cells ± SEM in cells treated with DMSO, forskolin, PTHrP, or isoproterenol, *P < .05.