Skip to main content
. Author manuscript; available in PMC: 2020 Apr 12.
Published in final edited form as: Circ Res. 2019 Apr 12;124(8):1253–1265. doi: 10.1161/CIRCRESAHA.118.314567

Figure 8. Restoration of CXCL7 rescues reendothelialization.

Figure 8.

(A) Schematics of SMC-specific expression vectors expressing both PKCδ shRNA and CXCR2 ligand. (B) Representative Evans blue dye-stained carotid arteries harvested 21 days after angioplasty from Lenti-enSM22αgc-ZsGreen-shPKCδ-, Lenti-enSM22αgc-CXCL1-shPKCδ-, and Lenti-enSM22αgc-CXCL7-shPKCδ-treated rats. Boundaries of the injured areas are indicated by the dashed lines. Reendothelialization was determined by the percentage of Evans blue negative area over the total injured area using ImageJ software. Scale bar = 3 mm. Results are expressed as mean±SEM. n=3-6, *p<0.05, One-way ANOVA. (C) Proposed mechanisms through which SMCs facilitate endothelial regeneration. Vascular injury, which leads to endothelial denudation, increases PKCδ (↑ PKCδ). Activation of PKCδ causes SMC apoptosis and stimulates the production of paracrine factors including STAT3 activation-mediated CXCL7, which in turn triggers migration of neighboring ECs to the denuded region.