Figure 6. CXCR2 ligands function downstream from PKCδ in the recruitment of ECs.

(A) Representative images of CXCL7 stained rat carotid cross-sections harvested from injured Lenti-enSM22αgc-non-targeting shRNA-treated or injured Lenti-enSM22αgc-shPKCδ-treated rats (7 days post-angioplasty). Nuclei were indicated by positive stains with DAPI (blue). The locations of the internal and external elastic lamina defining boundaries of the media are shown as white dashed lines. Scale bar = 50 μm. (B) Representative images of CXCL7 stained rat carotid cross-sections harvested 3 days after angioplasty from injured AdNull-treated or injured AdPKCδ-infected rats. Nuclei were indicated by positive stains with DAPI (blue). The locations of the internal and external elastic lamina defining boundaries of the media are shown as white dashed lines. Scale bar = 50 μm. (C) Wound closure of mouse ECs cultured in medium conditioned by AdNull- or AdPKCδ-infected and PMA- (1nM) treated SMCs in the presence of IgG, neutralizing antibody anti-CXCL1, anti-CXCL7 or anti-CXCR2. ECs were labeled with CMFDA green fluorescence dye for visualization. Dashed lines indicate the cell-free gap right after the scratch. Scale bar = 50 μm (D) Quantification of endothelial wound closure, determined by the percentage of the recovered area over the total injured area using ImageJ software. Results are expressed as mean±SEM. n=3, *p<0.05, One-way ANOVA.