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Research Paper|Volume 13, Issue 10|pp 13926—13940

Peroxiredoxin II with dermal mesenchymal stem cells accelerates wound healing

Mei-Hua Jin1, Nan-Nan Yu1,2, Ying-Hua Jin3, Ying-Ying Mao1, Lin Feng1, Yue Liu1, Ai-Guo Wang4, Hu-Nan Sun1, Taeho Kwon5, Ying-Hao Han1
  • 1College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Daqing 163319, Heilongjiang, P.R. China
  • 2Department of Plasma Bioscience and Display, Plasma Bioscience Research Center, Applied Plasma Medicine Center, Kwangwoon University, Nowon-gu 01897, Seoul, Republic of Korea
  • 3Library and Information Center, College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Daqing 163319, Heilongjiang, P.R. China
  • 4Laboratory Animal Center, Dalian Medical University, Dalian 116044, Liaoning, P.R. China
  • 5Primate Resources Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Jeongeup-si 56216, Jeonbuk, Republic of Korea
* Equal contribution
Received: January 12, 2021Accepted: March 23, 2021Published: May 24, 2021
https://doi.org/10.18632/aging.202990

Copyright: © 2021 Jin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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 II−/− DMSCs than in Prx II+/+ DMSCs. In vitro stimulation with 10 μM H2O2 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.