Author + information
- Li Lufeng and
- Xiahui Zhao
To explore whether vascular endothelial groth factor (VEGF) can regulate the proliferation and migration in endothelial progenitor cells(EPCs) in viro and regulate homing, re-endothelialization, and intima hyperplasia in vivo through connexin 43 (Cx43).
Primary EPCs dereved from rat spleen were isolated and cultured, and different concentrations of VEGF(0, 10, 50ng/mL) were used to stimulate EPCs. Western blotting was employed to detect the expression of Cx43. fluorescence redistribution after photobleaching(FRAP) was adopted to detect the fluorescent intensity in EPCs. The effect of Cx43 on the proliferation of EPCs was determined by CCK-8 assay. Transwell migration assay was used to analyze the effect of Cx43 interference on the migration of EPCs. After carotid artery injury model was established EPCs homing, re-endothelialization and HE staining were evaluated by Fluorescence labeling tracer method, Evans blue method and HE staining method respectively.
VEGF can promote the expression of Cx43 (P＜0.05). VGEF can also promote the gap junction of adjacent EPCs induced by Cx43 (P＜0.05). VEGF can promote proliferation and migration induced by Cx43 (P＜0.05), however when Cx43 is suppressed, the proliferation and migration of EPCs are weaken (P＜0.05). In animal experiments, EPCs homing and re-endothelialization are significantly increased in VEGF group (P＜0.05). Compared with VEGF group, EPCs homing and re-endothelialization are decreased in the VEGF+siCx43 group (P 0.05). Intima hyperplasia is decreased in VEGF group (P＜0.05). Compared with VEGF group, Intima hyperplasia is increased in the VEGF+siCx43 group (P＜0.05).
VEGF can increase the expression of Cx43 in EPCs, which enhances the gap junction and thus promotes the proliferation and migration of EPCs. In animal experiments, VEGF can promote EPCs homing and re-endothelialization and also suppresss intima hyperplasia.