ID 112327
著者
Tanigawa, Hiroki Kumamoto University
Miyata, Keishi Kumamoto University
Tian, Zhe Kumamoto University
Aoi, Jun Kumamoto University
Kadomatsu, Tsuyoshi Kumamoto University
Fukushima, Satoshi Kumamoto University
Ogata, Aki Kumamoto University
Takeda, Naoki Kumamoto University
Zhao, Jiabin Kumamoto University
Zhu, Shunshun Kumamoto University
Terada, Kazutoyo Kumamoto University
Endo, Motoyoshi Kumamoto University
Morinaga, Jun Kumamoto University
Sugizaki, Taichi Kumamoto University
Sato, Michio Kumamoto University
Morioka, Masaki Suimye University of Tokyo
Manabe, Ichiro University of Tokyo
Mashimo, Youichi Chiba University
Hata, Akira Chiba University
Taketomi, Yoshitaka Tokyo Metropolitan Institute of Medical Science
山本, 圭 Tokyo Metropolitan Institute of Medical Science|Tokushima University 徳島大学 教育研究者総覧 KAKEN研究者をさがす
Murakami, Makoto Tokyo Metropolitan Institute of Medical Science
Araki, Kimi Kumamoto University
Jinnin, Masatoshi Kumamoto University
Ihn, Hironobu Kumamoto University
Oike, Yuichi Kumamoto University
資料タイプ
学術雑誌論文
抄録
Psoriasis is a chronic inflammatory skin disease marked by aberrant tissue repair. Mutant mice modeling psoriasis skin characteristics have provided useful information relevant to molecular mechanisms and could serve to evaluate therapeutic strategies. Here, we found that epidermal ANGPTL6 expression was markedly induced during tissue repair in mice. Analysis of mice overexpressing ANGPTL6 in keratinocytes (K14-Angptl6 Tg mice) revealed that epidermal ANGPTL6 activity promotes aberrant epidermal barrier function due to hyperproliferation of prematurely differentiated keratinocytes. Moreover, skin tissues of K14-Angptl6 Tg mice showed aberrantly activated skin tissue inflammation seen in psoriasis. Levels of the proteins S100A9, recently proposed as therapeutic targets for psoriasis, also increased in skin tissue of K14-Angptl6 Tg mice, but psoriasis-like inflammatory phenotypes in those mice were not rescued by S100A9 deletion. This finding suggests that decreasing S100A9 levels may not ameliorate all cases of psoriasis and that diverse mechanisms underlie the condition. Finally, we observed enhanced levels of epidermal ANGPTL6 in tissue specimens from some psoriasis patients. We conclude that the K14-Angptl6 Tg mouse is useful to investigate psoriasis pathogenesis and for preclinical testing of new therapeutics. Our study also suggests that ANGPTL6 activation in keratinocytes enhances psoriasis susceptibility.
掲載誌名
Scientific Reports
ISSN
20452322
出版者
Springer Nature
6
開始ページ
34690
発行日
2016-10-04
備考
Supplementary Information : srep_6_34690_s1.pdf
権利情報
© The Author(s) 2016
This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
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出版社版DOI
出版社版URL
フルテキストファイル
言語
eng
著者版フラグ
出版社版
部局
生物資源系