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Title: Aquaporin-3 potentiates allergic airway inflammation in ovalbumin-induced murine asthma
Authors: Ikezoe, Kohei
Oga, Toru
Honda, Tetsuya
Hara-Chikuma, Mariko
Ma, Xiaojun
Tsuruyama, Tatsuaki  kyouindb  KAKEN_id
Uno, Kazuko
Fuchikami, Jun Ichi
Tanizawa, Kiminobu  kyouindb  KAKEN_id
Handa, Tomohiro  kyouindb  KAKEN_id
Taguchi, Yoshio
Verkman, Alan S.
Narumiya, Shuh
Mishima, Michiaki
Chin, Kazuo
Author's alias: 池添, 浩平
小賀, 徹
本田, 哲也
竹馬, 真理子
鶴山, 竜昭
谷澤, 公伸
半田, 知宏
成宮, 周
三嶋, 理晃
陳, 和夫
Issue Date: 11-May-2016
Publisher: Nature Publishing Group
Journal title: Scientific Reports
Volume: 6
Thesis number: 25781
Abstract: Oxidative stress plays a pivotal role in the pathogenesis of asthma. Aquaporin-3 (AQP3) is a small transmembrane water/glycerol channel that may facilitate the membrane uptake of hydrogen peroxide (H[2]O[2]). Here we report that AQP3 potentiates ovalbumin (OVA)-induced murine asthma by mediating both chemokine production from alveolar macrophages and T cell trafficking. AQP3 deficient (AQP3[-/-]) mice exhibited significantly reduced airway inflammation compared to wild-type mice. Adoptive transfer experiments showed reduced airway eosinophilic inflammation in mice receiving OVA-sensitized splenocytes from AQP3[-/-] mice compared with wild-type mice after OVA challenge, consistently with fewer CD4[+]T cells from AQP3[-/-] mice migrating to the lung than from wild-type mice. Additionally, in vivo and vitro experiments indicated that AQP3 induced the production of some chemokines such as CCL24 and CCL22 through regulating the amount of cellular H[2]O[2] in M2 polarized alveolar macrophages. These results imply a critical role of AQP3 in asthma, and AQP3 may be a novel therapeutic target.
Rights: 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
DOI(Published Version): 10.1038/srep25781
PubMed ID: 27165276
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