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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 2. C-type natriuretic peptide increases scratch closure and tubule formation in murine pulmonary microvascular endothelial cells via natriuretic peptide receptor-C.

Figure 2

(A) Migration (i.e. scratch closure) of murine pulmonary microvascular endothelial cells (PMEC) from wild type (WT) mice is facilitated by C-type natriuretic peptide (CNP; 1 nM) in a similar manner to vascular endothelial growth factor (VEGF; 30 ng/mL; n=6), (B) PMEC migration is impaired in cells from endothelium-specific CNP knockout (ecCNP-/-) mice compare to WT littermates (n=6), but (C) can be reversed by pharmacological addition of CNP (1 nM; n=6), (D) PMEC migration is arrested in cells from global natriuretic peptide receptor-C knockout (NPR-C-/-) but not global NPR-B-/- animals (n=6), (E & F) CNP (1 nM) augments PMEC migration in cells from NPR-B-/-, but not NPR-C-/- mice (n=6), (G & H) Intrinsic tubule forming capacity in PMEC is impaired in cells from ecCNP-/- and NPR-C-/-, but not NPR-B-/-, mice whereas CNP (1 nM) promotes tubule formation in WT, ecCNP-/- and NPR-B-/- PMEC but is unable to do so in NPR-C-/- cells (scale bars, 100 μm; n=12-15). Data are presented as mean ± SEM. Statistical analyses by (A-F) two-way ANOVA or (G) one-way ANOVA with Bonferroni post hoc test. *P<0.05, ***P<0.001 versus WT or absence of CNP (A-F), *P<0.05, ***P<0.001 versus WT or #P<0.05 versus corresponding genotype in the absence of CNP (G).