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Umbilical Cord Mesenchymal Stem Cell-Derived Exosomes Preserve Melanocyte Stem Cell Integrity Under Acute Neurogenic Oxidative Stress via Activation of the Nrf2-ARE Pathway in C57BL/6J Mice
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DOI：10.1111/jocd.70854.png)
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Abstract
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Background Stress-induced hair depigmentation is closely associated with neurogenic oxidative stress and dysfunction of melanocyte stem cells. Activation of antioxidant defense pathways, particularly the Nrf2-ARE pathway, may protect melanocytes from oxidative damage.Aims To investigate whether exosomes derived from human umbilical cord mesenchymal stem cells (HUCB-MSC-Exo) preserve melanocyte stem cell integrity under acute neurogenic oxidative stress through activation of the Nrf2-ARE pathway.Patients/Methods HUCB-MSC-Exo were characterized by transmission electron microscopy and the expression of exosomal markers CD63 and CD81. Melan-a cells were treated with exosomes at concentrations ranging from 0.50 & times; 108 to 2.0 & times; 108 particles/mL to assess cell proliferation. Nrf2 signaling and downstream antioxidant genes (HO-1, SOD-1, GR-1, and CAT) were evaluated using RT-PCR and western blotting, and intracellular calcium levels were measured. In vivo, acute neurogenic oxidative stress was induced in C57BL/6J mice using resiniferatoxin, followed by exosome treatment. Hair pigmentation, skin and follicle morphology, and antioxidant protein expression were assessed.Results HUCB-MSC-Exo promoted Melan-a cell proliferation in a dose-dependent manner, with increases of 53% and 94% at 1.5 & times; 108 and 2.0 & times; 108 particles/mL, respectively. Exosome treatment significantly upregulated Nrf2 and its downstream antioxidant genes and activated a calcium-dependent signaling pathway. In vivo, HUCB-MSC-Exo reduced stress-induced hair depigmentation, increased dermal thickness, lengthened hair shafts, improved follicular morphology, and enhanced antioxidant protein expression.Conclusions HUCB-MSC-Exo alleviates acute neurogenic oxidative stress and preserves melanocyte function by activating the Nrf2-ARE pathway, thereby mitigating stress-induced hair depigmentation in C57BL/6J mice.
Keywords:
Exosome
Hair follicles
Hair graying
Nrf2-ARE pathway
Resinferation
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J
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2.5
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