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首页> 外文期刊>The Journal of investigative dermatology. >Dissecting Wnt Signaling for Melanocyte Regulation during Wound Healing
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Dissecting Wnt Signaling for Melanocyte Regulation during Wound Healing

机译：对伤口愈合过程中黑色细胞调节的WNT信号传导

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摘要

Abnormal pigmentation is commonly seen in the wound scar. Despite advancements in the research of wound healing, little is known about the repopulation of melanocytes in the healed skin. Previous studies have shown the capacity of melanocyte stem cells in the hair follicle to contribute skin epidermal melanocytes after injury in mice and humans. Here, we focused on the Wnt pathway, known to be a vital regulator of melanocyte stem cells in efforts to better understand the regulation of follicle-derived epidermal melanocytes during wound healing. We showed that transgenic expression of Wnt inhibitor Dkk1 in melanocytes reduced epidermal melanocytes in the wound scar. Conversely, forced activation of Wnt signaling by genetically stabilizing beta-catenin in melanocytes increases epidermal melanocytes. Furthermore, we show that deletion of Wntless (Wls), a gene required for Wnt ligand secretion, within epithelial cells results in failure in activating Wnt signaling in adjacent epidermal melanocytes. These results show the essential function of extrinsic Wnt ligands in initiating Wnt signaling in follicle-derived epidermal melanocytes during wound healing. Collectively, our results suggest the potential for Wnt signal regulation to promote melanocyte regeneration and provide a potential molecular window to promote proper melanocyte regeneration after wounding and in conditions such as vitiligo.
机译：在伤口疤痕中通常看到异常色素沉着。尽管伤口愈合研究进展，但关于愈合皮肤中黑色素细胞的重新灌注很少。以前的研究表明，黑色素细胞干细胞在毛囊中的能力在小鼠和人类损伤后贡献皮肤表皮细胞。在这里，我们专注于WNT途径，已知是黑素细胞干细胞的重要调节剂，以更好地了解伤口愈合期间卵泡衍生的表皮黑色细胞的调节。我们表明，WNT抑制剂DKK1在黑素细胞中的转基因表达在伤口瘢痕中减少表皮黑色细胞。相反，通过在黑色细胞中遗传稳定β-连环蛋白的基因稳定β-连环蛋白的强制激活增加表皮黑色细胞。此外，我们表明，在上皮细胞内缺失Wntless（WLS），Wnt配体分泌所需的基因，导致在相邻表皮黑色细胞中激活Wnt信号传导。这些结果表明了在伤口愈合期间在卵泡衍生的表皮细胞细胞中启动WNT信号传导中的外部Wnt配体的基本函数。统称，我们的结果表明WNT信号调节的可能性，以促进黑素细胞再生，并提供潜在的分子窗，以促进伤害后的适当的黑素细胞再生，如白癜风。

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