Abstract
Previous studies found that hypoxic pretreatment of endothelial progenitor cells (EPCs) prior to transplantation had a greater therapeutic effect than untreated EPCs in promoting diabetic wound healing. However, the exact mechanism is uncertain. Here, circRNA expression in EPCs after hypoxic treatment was investigated. High-throughput sequencing was used to assess abnormal expression by EPCs of circular RNAs (circRNAs) following hypoxic pretreatment. Additionally, an in vivo full-thickness skin defect mouse model was used to assess the effects of transplanted EPCs on diabetic wound closure. Subsequently, the regulatory mechanism and targets were studied. The results showed that circ-Klhl8 overexpression suppressed hyper glucose-induced endothelial cell damage by activating autophagy. MiR-212-3p and SIRT5 were identified as the downstream targets of circ-Klhl8. Circ-Klhl8 overexpression promoted skin wound healing by regulating SIRT5-mediated autophagy. In conclusion, the study found that circ-Klhl8 overexpression increased the EPC therapeutic effect in promoting diabetic wound healing by targeting the miR-212-3p/SIRT5 axis.
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