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

间充质干细胞 Wnt信号通路 斑秃 毛囊 活力测定 癌症研究 干细胞 细胞生物学 生物 信号转导 医学 细胞 免疫学 生物化学
作者
Jung Eun Kim,Jee Hye Oh,Young Jun Woo,Ji Hee Jung,Kwan Ho Jeong,Hoon Kang
出处
期刊:Experimental Dermatology [Wiley]
卷期号:29 (3): 265-272 被引量:26
标识
DOI:10.1111/exd.13812
摘要

Abstract Mesenchymal stem cell therapy ( MSCT ) has been suggested as a new therapeutic strategy for immunological disorders. There have been only a few attempts to treat alopecia areata ( AA ) with MSCT . MSCT efficacy and mechanism of action in treating AA are not known. We sought to investigate the effect of human hematopoietic mesenchymal stem cells ( hHMSC s) 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 ( hDPC s) with interferon gamma ( IFN ‐γ). hHMSC s were administered to the hDPC s, and cell viability was determined. Similar studies were also conducted with human hair follicles (HFs) in culture. The change in expression of the Wnt/β‐catenin pathway and JAK / STAT pathway‐related molecules and growth factors in hHMSC ‐treated hDPC s was also examined by reverse transcription‐ PCR , Western blot assay and growth factor array. Immune privilege–related molecules were examined by immunohistochemistry in HF culture models. hHMSC s enhanced the cell viability of the hDPC s. hHMSC s activated several molecules in the Wnt/β‐catenin signalling pathway, including ß‐catenin and phosphorylated GSK 3b, and decreased IFN ‐γ‐induced expression of DKK 1 in hDPC s. hHMSC s suppressed IFN ‐γ‐induced expression of caspase‐1, caspase‐3 and IFN ‐γ receptor. hHMSC s induced the phosphorylation of STAT 1 and STAT 3 compared to controls and IFN ‐γ–pretreated hDPC s. hHMSC ‐treated HFs enhanced several growth factor mRNA s. hHMSC pretreatment modulated IFN ‐γ–induced expression of molecules related to HF immune privilege on HFs in organ culture. These data suggest MSCT may be a new potential therapeutic option in treating AA.
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