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Deletion of NAD(P)H Oxidase 2 Prevents Angiotensin II-Induced Skeletal Muscle Atrophy

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Title: Deletion of NAD(P)H Oxidase 2 Prevents Angiotensin II-Induced Skeletal Muscle Atrophy
Authors: Kadoguchi, Tomoyasu Browse this author
Takada, Shingo Browse this author →KAKEN DB
Yokota, Takashi Browse this author →KAKEN DB
Furihata, Takaaki Browse this author →KAKEN DB
Matsumoto, Junichi Browse this author
Tsuda, Masaya Browse this author
Mizushima, Wataru Browse this author
Fukushima, Arata Browse this author →KAKEN DB
Okita, Koichi Browse this author →KAKEN DB
Kinugawa, Shintaro Browse this author →KAKEN DB
Issue Date: 2-Jan-2018
Publisher: Hindawi
Journal Title: BioMed Research International
Volume: 2018
Start Page: 3194917
Publisher DOI: 10.1155/2018/3194917
Abstract: Skeletal muscle atrophy is induced by an imbalance between protein synthesis and degradation. Our previous studies reported that angiotensin II (AII) directly induced muscle atrophy in mice. This study investigated the role of NAD(P)H oxidase 2 (Nox2) activation by AII in the induction of skeletal muscle atrophy. For 4 weeks, either saline (vehicle: V) or AII (1000 ng kg(-1) min(-1)) was infused into male wild-type (WT) and Nox2 knockout (KO) mice via osmotic minipumps. Experiments were performed in the following 4 groups: WT + V, KO + V, WT + AII, and KO + AII. Body weight, muscle weight, and myocyte cross-sectional area were significantly decreased in WT + AII compared to WT + V mice, and these changes were not observed in KO + AII mice. Akt phosphorylation of Ser473 and p70S6K of Thr389 was decreased, gene expression levels of MuRF-1 and atrogin-1 were increased in WT + AII compared to WT + V, and these changes were significantly attenuated in KO + AII mice. The deletion of Nox2 prevented AII-induced skeletal muscle atrophy via improving the balance between protein synthesis and degradation. Therefore, Nox2 may be a therapeutic target for AII-induced skeletal muscle atrophy.
Rights: http://creativecommons.org/licenses/by/4.0/
Type: article
URI: http://hdl.handle.net/2115/68453
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 絹川 真太郎

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