RRC ID 49250
Author Watanabe M, Natsuga K, Nishie W, Kobayashi Y, Donati G, Suzuki S, Fujimura Y, Tsukiyama T, Ujiie H, Shinkuma S, Nakamura H, Murakami M, Ozaki M, Nagayama M, Watt FM, Shimizu H.
Title Type XVII collagen coordinates proliferation in the interfollicular epidermis.
Journal Elife
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.
Volume 6
Published 2017-7-11
DOI 10.7554/eLife.26635
PII e26635
PMID 28693719
PMC PMC5505703
MeSH Animals Autoantigens / genetics Autoantigens / metabolism* Cell Proliferation* Epidermis / physiology* Humans Mice Mice, Knockout Mice, Transgenic Non-Fibrillar Collagens / genetics Non-Fibrillar Collagens / metabolism* Wnt Signaling Pathway
IF 7.08
Times Cited 27
Mice RBRC05918