Exosomes from human umbilical cord mesenchymal stem cells promote the growth of human hair dermal papilla cells

  • PLoS One. 2025 Apr 30;20(4):e0320154. doi: 10.1371/journal.pone.0320154.
Yu-Cheng Chen  1  2 Wei-Cheng Tsai  3 Zhi-Xiang Li  3 Wan-Jung Lin  3 Hao-Yu Lin  3 Yi-Ju Hsieh  3 Kai-Hsuan Wang  3 You-Yan Chen  4 Tsong-Long Hwang  1  2  5  6  7 Tzou-Yien Lin  8
Affiliations
  • 1. Center for Drug Research and Development, College of Human Ecology, Chang Gung University of Science and Technology, Taoyuan, Taiwan.
  • 2. Graduate Institute of Health Industry Technology, College of Human Ecology, Chang Gung University of Science and Technology, Taoyuan, Taiwan.
  • 3. ExoOne Bio Co., Ltd., Taipei City, Taiwan.
  • 4. School of Traditional Chinese Medicine, College of Medicine, Chang Gung University, Taoyuan, Taiwan.
  • 5. Department of Chemical Engineering, Ming Chi University of Technology, New Taipei City, Taiwan.
  • 6. Graduate Institute of Natural Products, College of Medicine, Chang Gung University, Taoyuan, Taiwan.
  • 7. Department of Anesthesiology, Chang Gung Memorial Hospital, Taoyuan, Taiwan.
  • 8. Department of Paediatrics, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taoyuan, Taiwan.
Abstract

Human hair dermal papilla cells (HHDPCs) play a significant role in hair growth. This study found that human umbilical cord mesenchymal stem cell-derived exosomes (UC-MSC-Es) effectively enhanced cell growth of HHDPCs. UC-MSC-Es has a size range of 30-180 nm and expression of CD9, CD63, CD81, CD73, and TSG101. UC-MSC-Es significantly increased cell populations of HHDPCs in the S and G2/M phases. UC-MSC-Es also increased the expression of cell cycle-related proteins, β-catenin, and cyclin D1. Further mechanistic studies demonstrated that UC-MSC-Es promoted the phosphorylation of Akt and GSK-3β, and the inhibition of PI3K and Akt reduced the proliferative effects of UC-MSC-Es. Collectively, these findings suggest that UC-MSC-Es have a potential effect in treating hair loss through modulating PI3K and Akt-dependent pathways in HHDPCs.

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