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J Invest Dermatol. 2018 Jul;138(7):1591-1600. doi: 10.1016/j.jid.2018.01.030. Epub 2018 Feb 8.

Dissecting Wnt Signaling for Melanocyte Regulation during Wound Healing.

Author information

1
The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York, New York, USA; The Department of Cell Biology, New York University School of Medicine, New York, New York, USA.
2
Department of Pharmacology, Kyoto University, Sakyo, Kyoto, Japan.
3
Department of Dermatology, Yale Cancer Center, Yale School of Medicine, New Haven, Connecticut, USA.
4
Departments of Dermatology and Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
5
The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York, New York, USA; The Department of Cell Biology, New York University School of Medicine, New York, New York, USA. Electronic address: mayumi.ito@nyumc.org.

Abstract

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 β-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.

PMID:
29428355
PMCID:
PMC6019608
DOI:
10.1016/j.jid.2018.01.030
[Indexed for MEDLINE]
Free PMC Article

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