Fig. 8: CAMK1 contributes to phosphorylation of PINK1 and PARK2 to PTV-induced mitophagy. EPCs were stably transfected with Camk1 knockdown lentiviral vector 72 h before 0.5 μm PTV treatment for 24 h. | Communications Biology

Fig. 8: CAMK1 contributes to phosphorylation of PINK1 and PARK2 to PTV-induced mitophagy. EPCs were stably transfected with Camk1 knockdown lentiviral vector 72 h before 0.5 μm PTV treatment for 24 h.

From: Pitavastatin activates mitophagy to protect EPC proliferation through a calcium-dependent CAMK1-PINK1 pathway in atherosclerotic mice

Fig. 8

a Immunoblot was employed to detect phosphorylation of PINK1 Ser228 and PARK2 Ser65 in each group. We normalized the expression of total PINK1 or PARK2 to compare the phosphorylation level. b Quantitative analysis revealed that PTV significantly up-regulated Ser228 phosphorylation in PINK1 but Camk1 knockdown remarkably reduced this effect in PECs from atherosclerotic mice. c Quantitative analysis revealed that PTV significantly increased PARK2 Ser65 phosphorylation but Camk1 knockdown reversed this effect in PECs from atherosclerotic mice. d PTV treatment reversed HFD8w-induced mitochondrial swelling and rupture of mitochondrial cristae; either PINK1 or ATG7 silencing blocked the effect of PTV on mitochondria of EPCs. e PTV treatment reversed HFD8w-induced ROS production, scale bar: 10 μm. f PTV treatment reversed HFD 8w-induced MMP decreased, scale bar: 10 μm. Quantitative analysis indicated the effect of PTV on ROS (g) and MMP (h) of EPCs can be inhibited by silencing ATG7, PINK1 blocked, and 3-MA pretreatment. (EPCs were isolated from 3 ApoE−/− mice fed with high fat diet for 8 weeks and 3 independent experiments were performed, mean ± SD, *P < 0.05, **P < 0.01).

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