Fig. 5.

Endothelial cell delta-like protein-4 (Dll4) deficiency augments myosin light chain (MLC) phosphorylation and arterial force generation. A: aortic (Ao) segments from tamoxifen-treated control [vascular endothelial cadherin-Cre^ERT2 [VeCad-Cre^ERT2 (Ve)]⁻/Dll4 flox/flox (Dll4^f/f)] and Dll4-deficient (Ve⁺Dll4^def) mice subjected to myography. Graphs display constrictor responses to KCl (left) and phenylephrine (PE, right). Data represent means ± SE (n = 5). Data for KCl were analyzed using a t-test, *P = 0.0126; data for PE were analyzed using two-way ANOVA with Bonferroni’s post hoc test, *P < 0.05 and **P < 0.01. B: augmented mesenteric artery (MA) force production in response to depolarization (KCl, left) or agonists [phenylephrine (PE, middle) and angiotensin II (ANG II, right)] with Dll4 deficiency (Ve⁺Dll4^def) versus controls (Ve⁻Dll4^f/f). Myography data represent means ± SE. Data for KCl (n = 5) were analyzed using a t-test, *P = 0.0125; data for PE (n = 5) and ANG II (n = 4) were analyzed using two-way ANOVA with Bonferroni’s post hoc test, *P < 0.05, **P < 0.001, and ***P < 0.01. C: aortic segments treated with KCl or ANG II for 10 min (10′). Representative protein blots demonstrated enrichment of phosphorylated MLC (p-MLC) relative to total MLC (T-MLC) and β-actin in Dll4-deficient rings (Ve⁺Dll4^def) versus controls (Ve⁻Dll4^f/f). Densitometric data represent means ± SE (n = 3) normalized to Ve⁻Dll4^f/f and were analyzed using a t-test, *P = 0.0224 and **P = 0.0164. D: Ca²⁺ permeabilization and force generation experiments. MAs from control and tamoxifen-treated VeCad-Cre^ERT2+/Dll4^f/f (Ve⁺Dll4^def) mice were permeabilized with α-toxin and exposed to incremental Ca²⁺ concentrations. Myograph data are expressed as tension generated above set baseline at pCa 9. Data represent means ± SE (n = 4 per group) and were analyzed using a two-way ANOVA with Bonferroni’s post hoc test, *P < 0.005 and **P < 0.001.