Peroxiredoxin II with dermal mesenchymal stem cells accelerates wound healing
Meihua Jin, Nan‐Nan Yu, Yinghua Jin, Yingying Mao, Feng Lin, Yue Liu, Aiguo Wang, Hu‐Nan Sun, Taeho Kwon, Ying‐Hao Han
Abstract
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 IIâ/â DMSCs than in Prx II+/+ DMSCs. In vitro stimulation with 10 μM H2O2 significantly increased apoptosis in Prx IIâ/â DMSCs compared with Prx II+/+ DMSCs. The mRNA expression levels of EGF, b-FGF, PDGF-B, and VEGF did not significantly differ between Prx IIâ/â and Prx II+/+ DMSCs. Fibroblasts proliferated comparably when treated with Prx II+/+ DMSC-CM or Prx IIâ/â DMSC-CM. Wound healing was significantly higher in the Prx IIâ/â 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 IIâ/â 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.