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Wnt/beta-Catenin Signaling Stabilizes Hemidesmosomes in Keratinocytes

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Title: Wnt/beta-Catenin Signaling Stabilizes Hemidesmosomes in Keratinocytes
Authors: Kosumi, Hideyuki Browse this author
Watanabe, Mika Browse this author
Shinkuma, Satoru Browse this author
Nohara, Takuma Browse this author
Fujimura, Yu Browse this author
Tsukiyama, Tadasuke Browse this author →KAKEN DB
Donati, Giacomo Browse this author
Iwata, Hiroaki Browse this author →KAKEN DB
Nakamura, Hideki Browse this author
Ujiie, Hideyuki Browse this author →KAKEN DB
Natsuga, Ken Browse this author →KAKEN DB
Issue Date: Jun-2022
Publisher: Elsevier
Journal Title: Journal of investigative dermatology
Volume: 142
Issue: 6
Start Page: 1576
End Page: 1586 e2
Publisher DOI: 10.1016/j.jid.2021.10.018
Abstract: Hemidesmosomes (HDs) are adhesion complexes that promote epithelial-stromal attachment in stratified and complex epithelia, including the epidermis. In various biological processes, such as differentiation and migration of epidermal keratinocytes during wound healing or carcinoma invasion, quick assembly and disassembly of HDs are prerequisites. In this study, we show that inhibition of Wnt/0-catenin signaling disturbs HD organization in keratinocytes. Screening with inhibitors identified the depletion of HD components and HD-like structures through Wnt inhibition, but keratinocyte differentiation was not affected. Wnt inhibition significantly diminished plectin and type XVII collagen expression in the basal side of Wnt-inhibited cells and the dermo-epidermal junction of the Wnt-inactive murine basal epidermis. Similar to Wnt inhibition, PLEC- knockout cells or cells with plectin-type XVII collagen binding defects showed type XVII collagen reduction in the basal side of the cells, implying the possible involvement of Wnt/beta-catenin signaling in HD assembly. Atypical protein kinase C inhibition ameliorated the phenotypes of Wnt-inhibited cells. These findings show that Wnt/beta-catenin signaling regulates the localization of HD components in keratinocytes and that the atypical protein kinase C pathway is involved in Wnt inhibition-induced HD disarrangement. Our study suggests that the Wnt signaling pathway could be a potential therapeutic target for treating HD-defective diseases, such as epidermolysis bullosa.
Rights: © 2021. This manuscript version is made available under the CC-BY-NC-ND 4.0 license
Type: article (author version)
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 夏賀 健

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