Wnt/beta-Catenin Signaling Stabilizes Hemidesmosomes in Keratinocytes

Kosumi, Hideyuki; Watanabe, Mika; Shinkuma, Satoru et al.

Journal of investigative dermatology, 2022, 142(6), 1576-1586 e2

Permalink : https://hdl.handle.net/2115/89791

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アクセス権
open access
URI
https://hdl.handle.net/2115/89791
タイトル
Wnt/beta-Catenin Signaling Stabilizes Hemidesmosomes in Keratinocytes
著者
Kosumi, Hideyuki ; Watanabe, Mika ; Shinkuma, Satoru ; Nohara, Takuma ; Fujimura, Yu ; Tsukiyama, Tadasuke ; Donati, Giacomo ; Iwata, Hiroaki ; Nakamura, Hideki ; Ujiie, Hideyuki ; Natsuga, Ken
著者名
Kosumi, Hideyuki
著者名
Watanabe, Mika
著者名
Shinkuma, Satoru
著者名
Nohara, Takuma
著者名
Fujimura, Yu
e-Rad_Researcher
20399819
著者名
Tsukiyama, Tadasuke
著者名
Donati, Giacomo
e-Rad_Researcher
20397334
著者名
Iwata, Hiroaki
著者名
Nakamura, Hideki
e-Rad_Researcher
60374435
著者名
Ujiie, Hideyuki
e-Rad_Researcher
70645457
著者名
Natsuga, Ken
言語
英語
発行日
2022-06
出版者
Elsevier
収録物名
Journal of investigative dermatology
巻(号)
142(6)
ページ
1576-1586 e2
抄録
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.
資源タイプ
学術雑誌論文
出版タイプ
Accepted Manuscript
権利情報
Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
権利情報
© 2021. This manuscript version is made available under the CC-BY-NC-ND 4.0 license https://creativecommons.org/licenses/by-nc-nd/4.0/
PISSN
0022-202X
関連情報 (isVersionOf)
出版社版DOI
https://doi.org/10.1016/j.jid.2021.10.018