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. Author manuscript; available in PMC: 2020 Mar 26.
Published in final edited form as: Circulation. 2019 Mar 26;139(13):1612–1628. doi: 10.1161/CIRCULATIONAHA.118.036344

Figure 3. Aortic sprouting and matrigel plug neovascularization is diminished in vessels lacking either endothelial C-type natriuretic peptide or natriuretic pepide receptor-C.

Figure 3

(A-C) C-type natriuretic peptide (CNP; 1 pM – 1 μM) promotes de novo vessel sprouting ex vivo with a maximal effect equivalent to that produced by vascular endothelial growth factor (VEGF; 30 ng/mL; n=10), whereas inherent vessel sprouting capacity is diminished in aortic rings from endothelium-specific CNP knockout (ecCNP-/-) and global natriuretic peptide receptor-C knockout (NPR-C-/-), but not global NPR-B-/-, mice and the pro-angiogenic action of CNP (1 nM) is maintained in wild type (WT), ecCNP-/- and NPR-B-/- vessels but absent in NPR-C-/- aortae (n=6), (D) CNP (1 nM) facilitates neovascularisation of matrigel plugs in vivo in WT and ecCNP-/- mice but is unable to recapitulate this pro-angiogenic activity in NPR-C-/- animals (n=12), as interrogated by (E) hemoglobin content, (F) Hematoxylin and eosin (H&E; upper panel) and immunofluorescence (lower panel) staining of transverse sections of the excised matrigel plugs (DAPI nuclear stain, blue; endothelium marker isolectin B4, green; arrows denote overt endothelial staining; scale bars, 50 μm). Data are presented as mean ± SEM. Statistical analyses by one-way ANOVA with Bonferroni post hoc test. *P<0.05, **P<0.01 versus Control or WT and #P<0.05, ##P<0.01 versus corresponding genotype in the absence of CNP.