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. 2023 Aug 7;148(13):1023–1034. doi: 10.1161/CIRCULATIONAHA.123.065547

Figure 3.

Figure 3.

cGAS activation within the endothelium induces cGAMP-dependent vessel relaxation. A, Vasoconstriction to phenylephrine of isolated aorta treated with cGMP or cGAMP (n=4). B, VASP Ser239 phosphorylation in mouse aorta treated with cGAMP (n=4). C, Vasoconstriction to phenylephrine of isolated aorta treated with G3-YSD from WT or cGAS littermate mice (n=6). D, Vasoconstriction to phenylephrine of isolated aorta treated with G3-YSD in the presence or absence of the PKGI inhibitor RP-8-Br-cGMPS (n=5–6). E, Vasoconstriction to phenylephrine of isolated aorta treated with G3-YSD in the presence or absence of the soluble guanylate cyclase inhibitor ODQ (n=8). F, The abundance of cGAS (n=12), and VASP and TBK1 phosphorylation, as well, in intact and denuded mouse aorta treated with G3-YSD (n=4). G, Vasoconstriction to phenylephrine of intact or denuded aorta treated with G3-YSD (n=4–6). *P<0.05; **P<0.01; ***P<0.005. Comparisons were made using 1-way ANOVA (B, F) or 2-way ANOVA (A, C, D, E, G) followed by the Tukey post hoc test. cGAMP indicates cyclic GMP-AMP; cGAS, cyclic GMP-AMP synthase; Ctrl, control; KO, knockout; ODQ, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one; PE, phenylephrine; TBK1, TANK-binding kinase 1; VASP, vasodilator stimulated phosphoprotein; and WT, wild type.