Type XVII collagen coordinates proliferation in the interfollicular epidermis
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) prol...
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doaj-de5c2abe4d95455fbf4741ece75546102021-05-05T13:36:35ZengeLife Sciences Publications LtdeLife2050-084X2017-07-01610.7554/eLife.26635Type XVII collagen coordinates proliferation in the interfollicular epidermisMika Watanabe0Ken Natsuga1https://orcid.org/0000-0003-3865-6366Wataru Nishie2Yasuaki Kobayashi3Giacomo Donati4Shotaro Suzuki5Yu Fujimura6Tadasuke Tsukiyama7Hideyuki Ujiie8Satoru Shinkuma9Hideki Nakamura10Masamoto Murakami11Michitaka Ozaki12Masaharu Nagayama13Fiona M Watt14https://orcid.org/0000-0001-9151-5154Hiroshi Shimizu15Department of Dermatology, Hokkaido University Graduate School of Medicine, Sapporo, JapanDepartment of Dermatology, Hokkaido University Graduate School of Medicine, Sapporo, JapanDepartment of Dermatology, Hokkaido University Graduate School of Medicine, Sapporo, JapanCenter for Simulation Sciences, Ochanomizu University, Tokyo, JapanCentre for Stem Cells and Regenerative Medicine, King’s College London, London, United Kingdom; Department of Life Sciences and Systems Biology, University of Turin, Turin, ItalyDepartment of Dermatology, Hokkaido University Graduate School of Medicine, Sapporo, JapanDepartment of Dermatology, Hokkaido University Graduate School of Medicine, Sapporo, JapanDepartment of Biochemistry, Hokkaido University Graduate School of Medicine, Sapporo, JapanDepartment of Dermatology, Hokkaido University Graduate School of Medicine, Sapporo, JapanDepartment of Dermatology, Hokkaido University Graduate School of Medicine, Sapporo, Japan; Division of Dermatology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, JapanDepartment of Dermatology, Hokkaido University Graduate School of Medicine, Sapporo, JapanDepartment of Dermatology, Ehime University Graduate School of Medicine, Toon, JapanDepartment of Biological Response and Regulation, Faculty of Health Sciences, Hokkaido University, Sapporo, JapanResearch Institute for Electronic Science, Hokkaido University, Sapporo, JapanCentre for Stem Cells and Regenerative Medicine, King’s College London, London, United KingdomDepartment of Dermatology, Hokkaido University Graduate School of Medicine, Sapporo, JapanType 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.https://elifesciences.org/articles/26635extracellular matrixtissue homeostasisepidermis |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Mika Watanabe Ken Natsuga Wataru Nishie Yasuaki Kobayashi Giacomo Donati Shotaro Suzuki Yu Fujimura Tadasuke Tsukiyama Hideyuki Ujiie Satoru Shinkuma Hideki Nakamura Masamoto Murakami Michitaka Ozaki Masaharu Nagayama Fiona M Watt Hiroshi Shimizu |
spellingShingle |
Mika Watanabe Ken Natsuga Wataru Nishie Yasuaki Kobayashi Giacomo Donati Shotaro Suzuki Yu Fujimura Tadasuke Tsukiyama Hideyuki Ujiie Satoru Shinkuma Hideki Nakamura Masamoto Murakami Michitaka Ozaki Masaharu Nagayama Fiona M Watt Hiroshi Shimizu Type XVII collagen coordinates proliferation in the interfollicular epidermis eLife extracellular matrix tissue homeostasis epidermis |
author_facet |
Mika Watanabe Ken Natsuga Wataru Nishie Yasuaki Kobayashi Giacomo Donati Shotaro Suzuki Yu Fujimura Tadasuke Tsukiyama Hideyuki Ujiie Satoru Shinkuma Hideki Nakamura Masamoto Murakami Michitaka Ozaki Masaharu Nagayama Fiona M Watt Hiroshi Shimizu |
author_sort |
Mika Watanabe |
title |
Type XVII collagen coordinates proliferation in the interfollicular epidermis |
title_short |
Type XVII collagen coordinates proliferation in the interfollicular epidermis |
title_full |
Type XVII collagen coordinates proliferation in the interfollicular epidermis |
title_fullStr |
Type XVII collagen coordinates proliferation in the interfollicular epidermis |
title_full_unstemmed |
Type XVII collagen coordinates proliferation in the interfollicular epidermis |
title_sort |
type xvii collagen coordinates proliferation in the interfollicular epidermis |
publisher |
eLife Sciences Publications Ltd |
series |
eLife |
issn |
2050-084X |
publishDate |
2017-07-01 |
description |
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. |
topic |
extracellular matrix tissue homeostasis epidermis |
url |
https://elifesciences.org/articles/26635 |
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