Protective effects of human umbilical cord blood‑derived mesenchymal stem cells against dexamethasone‑induced apoptotic cell death in hair follicles

2019 
Alopecia is a common and distressing condition, and developing new therapeutic agents to prevent hair loss is important. Human umbilical cord bloodderived mesenchymal stem cells (hUCBMSCs) have been studied intensively in regenerative medicine. However, the therapeutic potential of these cells against hair loss and hair organ damage remains unclear, and the effects of hUCBMSC transplantation on hair loss require evaluation. The current study aimed to investigate the effects of hUCBMSCs on hair regression in vivo and restoration of anagen conduction on hair growth in vitro. The effects of hUCBMSCs were explored in mouse catagen induction models using a topical treatment of 0.1% dexamethasone to induce hair regression. Dexamethasone was also used to simulate a stress environment in vitro. The results demonstrated that hUCBMSCs significantly prevented hair regression induced by dexamethasone topical stimulation in vivo. Additionally, hUCBMSCs significantly increased the proliferation of human dermal papilla cells (hDPCs) and HaCaT cells, which are key constituent cells of the hair follicle. Stimulation of vascular endothelial growth factor secretion and decreased expression of DKK1 by hUCBMSCs were also observed in hDPCs. Restoration of cell viability by hUCBMSCs suggested that these cells exerted a protective effect on glucocorticoid stressassociated hair loss. In addition, antiapoptotic effects and regulation of the autophagic flux recovery were observed in HaCaT cells. The results of the present study indicated that hUCBMSCs may have the capacity to protect hair follicular dermal papilla cells and keratinocytes, thus preventing hair loss. Additionally, the protective effects of hUCBMSCs may be resistant to dysregulation of autophagy under harmful stress.
    • Correction
    • Source
    • Cite
    • Save
    • Machine Reading By IdeaReader
    0
    References
    2
    Citations
    NaN
    KQI
    []