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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 7. Reponses to vessel injury and wound healing in vivo are impaired in endothelium-specific C-type natriuretic peptide knockout and global natriuretic peptide receptor-C knockout mice.

Figure 7

(A-C) Neointimal hyperplasia (intima:media ratio) in response to wire injury in the carotid artery is exacerbated in endothelium-specific C-type natriuretic peptide knockout (ecCNP-/-) and global natriuretic peptide receptor-C knockout (NPR-C-/-) mice compared to wild type (WT) littermates (n=6-7). Representative images showing hematoxylin & eosin (H&E) staining, immunostaining with alpha smooth muscle actin (brown; panels 1-3, scale bar, 100μm) and immunofluorescence with DAPI nuclear stain (blue) and endothelium marker isolectin B4 (green; arrows denote overt endothelial staining; panels 4 & 5, scale bars, 50μm and 20μm, respectively). Wound healing (% closure) is impaired in (D & E) ecCNP-/- and (F & G) NPR-C-/- mice compared to WT littermates (n=9-13). Data are presented as mean ± SEM. Statistical analyses by (B & C) one-way ANOVA with Bonferroni post hoc test or (D, F & H) two-way ANOVA. *P<0.05, ***P<0.001 versus corresponding genotype uninjured and #P<0.05 versus WT injured (A) or *P<0.05, **P<0.01 versus WT (B).