Vitiligo is a refractory disfiguring skin disease. However, the aetiology and pathogenesis of vitiligo have not been fully defined. Previous studies have shown that exosomes from normal human keratinocytes improve melanogenesis by up‐regulating the expression of melanogenesis‐related proteins. Several microRNAs (miRNAs) have been demonstrated to be effective in modulating melanogenesis via exosomes. In the present study, it was found that the effect of exosomes derived from keratinocytes in vitiligo lesions in regulating melanin synthesis is weakened. Furthermore, miR‐200c was detected to be significantly down‐regulated in exosomes from keratinocytes in vitiligo lesions. In addition, miR‐200c enhanced the expression of melanogenesis‐related genes via suppressing SOX1 to activate β‐catenin. In conclusion, our study revealed that the effect of exosomes secreted by keratinocytes in vitiligo lesions exhibited a weaker capacity in promoting melanogenesis of melanocytes. Moreover, the expression of miR‐200c, which mediates melanogenesis in exosomes secreted by keratinocytes in vitiligo lesions, is down‐regulated, which may be one of the pathogenesis in vitiligo. Therefore, keratinocyte‐derived exosomal miR‐200c may be a potential target for the treatment of vitiligo.

中文翻译：

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白癜风病变中源自角质形成细胞的外泌体miR-200c的下调抑制了黑色素生成。

白癜风是一种难治性的毁容性皮肤病。但是，白癜风的病因和发病机制尚未完全确定。先前的研究表明，正常人角质形成细胞的外泌体可通过上调黑色素生成相关蛋白的表达来改善黑色素生成。几种微RNA（miRNA）已被证明可有效地通过外来体调节黑色素生成。在本研究中，发现白癜风病变中源自角质形成细胞的外来体在调节黑色素合成中的作用减弱。此外，在白癜风病变的角质形成细胞的外泌体中检测到miR-200c显着下调。此外，miR-200c通过抑制SOX1激活β-catenin增强了黑色素生成相关基因的表达。结论，我们的研究表明，角质形成细胞分泌的外来体在白癜风病变中的作用表现出较弱的促进黑色素细胞黑素生成的能力。此外，miR-200c的表达下调，它介导白癜风病变中角质形成细胞分泌的外泌体中黑色素的生成，这可能是白癜风的发病机理之一。因此，源自角质形成细胞的外泌体miR-200c可能是治疗白癜风的潜在靶标。