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Type XVII collagen coordinates proliferation in the interfollicular epidermis

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Title: Type XVII collagen coordinates proliferation in the interfollicular epidermis
Authors: Watanabe, Mika Browse this author
Natsuga, Ken Browse this author →KAKEN DB
Nishie, Wataru Browse this author →KAKEN DB
Kobayashi, Yasuaki Browse this author
Donati, Giacomo Browse this author
Suzuki, Shotaro Browse this author
Fujimura, Yu Browse this author
Tsukiyama, Tadasuke Browse this author →KAKEN DB
Ujiie, Hideyuki Browse this author →KAKEN DB
Shinkuma, Satoru Browse this author →KAKEN DB
Nakamura, Hideki Browse this author →KAKEN DB
Murakami, Masamoto Browse this author
Ozaki, Michitaka Browse this author →KAKEN DB
Nagayama, Masaharu Browse this author →KAKEN DB
Watt, Fiona M Browse this author
Shimizu, Hiroshi Browse this author →KAKEN DB
Issue Date: 11-Jul-2017
Publisher: eLife Sciences Publications
Journal Title: Elife
Volume: 6
Start Page: e26635
Publisher DOI: 10.7554/eLife.26635
Abstract: Type XVII collagen (COL17) is a transmembrane protein located at the epidermal basement membrane zone. COL17 deficiency results in premature hair aging phenotypes and in junctional epidermolysis bullosa. Here, we show that COL17 plays a central role in regulating interfollicular epidermis (IFE) proliferation. Loss of COL17 leads to transient IFE hypertrophy in neonatal mice owing to aberrant Wnt signaling. The replenishment of COL17 in the neonatal epidermis of COL17-null mice reverses the proliferative IFE phenotype and the altered Wnt signaling. Physical aging abolishes membranous COL17 in IFE basal cells because of inactive atypical protein kinase C signaling and also induces epidermal hyperproliferation. The overexpression of human COL17 in aged mouse epidermis suppresses IFE hypertrophy. These findings demonstrate that COL17 governs IFE proliferation of neonatal and aged skin in distinct ways. Our study indicates that COL17 could be an important target of anti-aging strategies in the skin.
Type: article
Appears in Collections:北海道大学病院 (Hokkaido University Hospital) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 夏賀 健

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OAI-PMH ( junii2 , jpcoar )


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