Effects of mesenchymal stem cell therapy on alopecia areata in cellular and hair follicle organ culture models.

Exp Dermatol. 2018 Oct 29. doi: 10.1111/exd.13812. [Epub ahead of print]
Effects of mesenchymal stem cell therapy on alopecia areata in cellular and hair follicle organ culture models.
Kim JE1, Oh JH1, Woo YJ1, Jung JH1, Jeong KH1, Kang H1.

Mesenchymal stem cell therapy (MSCT) has been suggested as a new therapeutic strategy for immunologic disorders. There have been only a few attempts to treat alopecia areata (AA) with MSCT. MSCT efficacy and mechanism of action in treating AA is not known. We sought to investigate the effect of human hematopoietic mesenchymal stem cells (hHMSCs) on an in vitro model of AA and to explore relevant mechanisms that regulate efficacy. An AA-like environment was induced by pretreatment of human dermal papilla cells (hDPCs) with interferon gamma (IFN-γ). hHMSCs were administered to the hDPCs and cell viability was determined. Similar studies were also conducted with human hair follicles in culture. The change of expression of the Wnt/β-catenin pathway and JAK-STAT pathway-related molecules and growth factors in hHMSC-treated hDPCs was also examined by reverse transcription PCR, Western blot assay and growth factor array. Immune-privilege related molecules were examined by immunohistochemistry in hair follicle culture models. hHMSCs enhanced the cell viability of the hDPCs. hHMSCs activated several molecules in the Wnt/β-catenin signaling pathway, including ß-catenin and phosphorylated GSK3b, and decreased IFN-γ-induced expression of DKK1 in hDPCs. hHMSCs suppressed IFN-γ-induced expression of caspase-1, 3, and IFN-γ receptor. hHMSCs induced the phosphorylation of STAT1 and STAT3 ompared to controls and IFN-γ pretreated hDPCs. hHMSC-treated hair follicles enhanced several growth factor mRNAs. hHMSC pre-treatment modulated IFN-γ-induced expression of molecules related to hair follicle immune privilege on hair follicles in organ culture. These data suggest MSCT may be anew potential therapeutic option in treating AA.

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