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. In vitro stimulation with 10 μM H(2)O(2) 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.