Fig. 9: Disrupting of CAMK1-mediated mitophagy prevents EPC-mediated repairment of vascular endothelium. | Communications Biology

Fig. 9: Disrupting of CAMK1-mediated mitophagy prevents EPC-mediated repairment of vascular endothelium.

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

Fig. 9

a EPCs tracing in vivo. pEGFP-N2-EPCs were pre-treated by 0.5 μM PTV for 24 h and labeled by acLDL-DiI. EPCs in PTV + shAtg7 group were received lentivirus transfection to knock down Atg7, and EPCs in PTV + shAtg7 groups were received lentivirus transfection to knock down Camk1, respectively. Then EPCs were injected into ApoE-/- mice after vascular injury and attached to the vascular injury site. EPCs homed to vascular endothelium exhibited both red (acLDL-DiI) and green (EGFP) fluorescence. More EPCs in PTV + VC group home to vascular injury site compared with those in PTV + shAtg7 and PTV + shCAMK1 groups. b Quantification of Evans blue staining showed that knocked down Atg7 (49.63 ± 6.20 %) or Camk1 (48.70 ± 6.62%) reduced reendothelialization area compared with those in PTV + VC groups (74.73 ± 5.68 %). VC, vector control. (EPCs were isolated from 3 normal mice. The figures represented 3 independent experiments; mean ± SD, **P < 0.01). c A schematic drawing of the calcium signal and mitophagy pathway in EPCs after PTV treatment. PTV elicits mitochondrial calcium release and increases [Ca2+]i that further phosphorylates CAMK1. CAMK1 phosphorylation serves as a PINK1 kinase to activate PINK1 and recruit as well as phosphorylates PARK2 to induce mitophagy. Mitophagy activation protects EPC proliferation by reducing mitochondrial ROS production and maintaining mitochondrial homeostasis in atherosclerosis.

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