Exosomes derived from human dental pulp stem cells increase flap survival with ischemia-reperfusion injuries.

To investigate the effect of hDPSC-Exos in flap I/R injury, a condition in which tissue damage increases after blood flow is restored to the flap after ischemia. HUVECs were used to investigate the influences and mechanisms of hDPSC-Exos on cell proliferation and migration. A rat model was established to verify the role of hDPSC-Exos in flap I/R injuries . hDPSC-Exos promoted the proliferation, migration and tube formation of HUVECs in a dose-dependent way by activating PI3K/AKT signaling pathway, and improved the survival and microvessel density of the flap and suppressed epithelial cell apoptosis. hDPSC-Exos can enhance flap repair after I/R injury. This process may be mediated by the activation of PI3K/AKT signaling pathway.