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2016 Fiscal Year Final Research Report

Molecular mechanisms of the itch sensation and skin inflammation induced by epidermal tight junction barrier deficiency

Research Project

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Project/Area Number 15K15422
Research Category

Grant-in-Aid for Challenging Exploratory Research

Allocation TypeMulti-year Fund
Research Field Dermatology
Research InstitutionKeio University

Principal Investigator

Kubo Akiharu  慶應義塾大学, 医学部(信濃町), 准教授 (70335256)

Co-Investigator(Renkei-kenkyūsha) KUBO Akiharu  理化学研究所, 統合生命医科学研究センター, チームリーダー (50452272)
Project Period (FY) 2015-04-01 – 2017-03-31
Keywordsタイトジャンクション / 皮膚バリア / かゆみ / アトピー性皮膚炎
Outline of Final Research Achievements

The stratum corneum (SC) and tight junctions (TJs) form physical barriers in the skin. A congenital TJ barrier defect caused by a deficiency of claudin-1, which encodes a major epidermal TJ adhesion molecule, results in early neonatal death in mice and neonatal ichthyosis-sclerosing cholangitis syndrome in humans. These observations suggest the essential role of TJs in skin homeostasis. Here, we established tamoxifen (TAM)-inducible epidermis-specific claudin-1 knockout mice (K14-creERT+/-, Cldn1flox/flox mice) and investigated the pathophysiology of epidermal TJ defects in adult mice. To clarify the barrier defects of the SC and TJ separately, we measured water evaporation through isolated SC sheets (WETIS) ex vivo.On day 8, claudin-1 staining disappeared, but no elevation of WETIS was observed. On day 18, compact hyperkeratosis and increased WETIS were observed, suggesting that the TJ barrier leakage secondarily induced the SC barrier defect.

Free Research Field

皮膚科学

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Published: 2018-03-22  

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