Peroxiredoxin II with dermal mesenchymal stem cells accelerates wound healing.

Peroxiredoxin II (Prx II) is involved in proliferation, differentiation, and aging in various cell types. However, Prx II-mediated stem cell regulation is poorly understood. Here, dermal mesenchymal stem cells (DMSCs), cell-growth factor-rich conditioned medium from DMSCs (DMSC-CM), and DMSC-derived exosomes (DMSC-Exos) were used to explore the regulatory role of Prx II in DMSC wound healing. Following treatment, wound healing was significantly decelerated in Prx II DMSCs than in Prx II DMSCs. stimulation with 10 μM HO significantly increased apoptosis in Prx II DMSCs compared with Prx II DMSCs. The mRNA expression levels of EGF, b-FGF, PDGF-B, and VEGF did not significantly differ between Prx II and Prx II DMSCs. Fibroblasts proliferated comparably when treated with Prx II DMSC-CM or Prx II DMSC-CM. Wound healing was significantly higher in the Prx II DMSC-Exos-treated group than in the Prx II DMSCs-Exos-treated group. Moreover, microRNA (miR)-21-5p expression levels were lower and miR-221 levels were higher in Prx II DMSCs than in Prx II DMSCs. Therefore, our results indicate that Prx II accelerated wound healing by protecting DMSCs from reactive oxygen species-induced apoptosis; however, Prx II did not regulate cell/growth factor secretion. Prx II potentially regulates exosome functions via miR-21-5p and miR-221.