Fig. 5: PINK1-PARK2 pathway contributed to EPC proliferation.

a Representative western blots showed that shRNA targeting Pink1 (shPink1) effectively silenced PINK1 protein expression and shRNA targeting Park2 (shPark2) effectively silenced PARK2 protein expression after 24 h infection, respectively. Representative western blots and quantitative analysis revealed that either silencing Pink1 (b, d) or Park2 (c, e) significantly reduced MAP1LC3B expression. CCK-8 assay showed that either silencing Pink1 (f) or Park2 (g) before PTV treatment significantly reduced proliferative activity compared with PTV alone group. h EPCs of silencing Pink1 were seeded on E-plates for 24 h, 0.5 μM PTV was added to E-plates in PTV and shPink1 + PTV groups after 24 h incubation (black arrow). The normalized cell index indicated that EPC proliferative activity decreased in shPink1 + PTV group compared with PTV alone group. i EPCs of silencing Park2 were seeded on E-plates for 24 h, 0.5 μM PTV was added to E-plates in PTV and shPark2 + PTV groups after 24 h incubation (black arrow). The normalized cell index indicated that EPC proliferative activity decreased in shPark2 + PTV group compared with PTV alone group. j Western blots of the expression of PINK1, PARK2 and their phosphorylated form in WT and Pink1^−/− mice. EPCs with or without 0.5 μM PTV treatment were seeded on E-plates for 24 h, 0.5 μM in PTV and Pink1^−/− + PTV groups after 24 h incubation. The normalized cell index (k) and CCK-8 (l) indicated that EPC proliferative activity fell down in WT and Pink1^−/− mice with or without PTV treatment. (EPCs were isolated from ApoE^−/− mice fed with high-fat diet for 8 weeks, cells were isolated from 3 mice for 1 experiment and 3 independent experiments were performed, mean ± SD, *P < 0.05, **P < 0.01).