神戸大学附属図書館デジタルアーカイブ
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学内刊行物
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https://hdl.handle.net/20.500.14094/90005448
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2024-04-19
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90005448 (fulltext)
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2.40 MB
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メタデータID
90005448
アクセス権
open access
出版タイプ
Accepted Manuscript
タイトル
Hearing vulnerability after noise exposure in a mouse model of reactive oxygen species overproduction
著者
Morioka, Shigefumi ; Sakaguchi, Hirofumi ; Yamaguchi, Taro ; Ninoyu, Yuzuru ; Mohri, Hiroaki ; Nakamura, Takashi ; Hisa, Yasuo ; Ogita, Kiyokazu ; Saito, Naoaki ; Ueyama, Takehiko
著者名
Morioka, Shigefumi
著者名
Sakaguchi, Hirofumi
著者名
Yamaguchi, Taro
著者名
Ninoyu, Yuzuru
著者名
Mohri, Hiroaki
著者名
Nakamura, Takashi
著者名
Hisa, Yasuo
著者名
Ogita, Kiyokazu
著者ID
A0754
研究者ID
1000060178499
KUID
https://kuid-rm-web.ofc.kobe-u.ac.jp/search/detail?systemId=5821517134b6cd81520e17560c007669
著者名
Saito, Naoaki
齋藤, 尚亮
サイトウ, ナオアキ
所属機関名
バイオシグナル総合研究センター
著者ID
A1239
研究者ID
1000080346254
KUID
https://kuid-rm-web.ofc.kobe-u.ac.jp/search/detail?systemId=443e05a0c3fc0358520e17560c007669
著者名
Ueyama, Takehiko
上山, 健彦
ウエヤマ, タケヒコ
所属機関名
バイオシグナル総合研究センター
収録物名
Journal of Neurochemistry
巻(号)
146(4)
ページ
459-473
出版者
Wiley
刊行日
2018-08
公開日
2019-09-01
抄録
Previous studies have convincingly argued that reactive oxygen species (ROS) contribute to the development of several major types of sensorineural hearing loss, such as noise-induced hearing loss (NIHL), drug-induced hearing loss, and age-related hearing loss. However, the underlying molecular mechanisms induced by ROS in these pathologies remain unclear. To resolve this issue, we established an in vivo model of ROS overproduction by generating a transgenic (TG) mouse line expressing the human NADPH oxidase 4 (NOX4, NOX4-TG mice), which is a constitutively active ROS-producing enzyme that does not require stimulation or an activator. Overproduction of ROS was detected at the cochlea of the inner ear in NOX4-TG mice, but they showed normal hearing function under baseline conditions. However, they demonstrated hearing function vulnerability, especially at high-frequency sounds, upon exposure to intense noise, which was accompanied by loss of cochlear outer hair cells (OHCs). The vulnerability to loss of hearing function and OHCs was rescued by treatment with the antioxidant Tempol. Additionally, we found increased protein levels of the heat-shock protein 47 (HSP47) in models using HEK293 cells, including H2O2 treatment and cells with stable and transient expression of NOX4. Furthermore, the up-regulated levels of Hsp47 were observed in both the cochlea and heart of NOX4-TG mice. Thus, antioxidant therapy is a promising approach for the treatment of NIHL. Hsp47 may be an endogenous antioxidant factor, compensating for the chronic ROS overexposure in vivo, and counteracting ROS-related hearing loss.
キーワード
antioxidant
hearing loss
Hsp47
NOX4
ROS
transgenic mouse model
カテゴリ
バイオシグナル総合研究センター
学術雑誌論文
権利
© 2018 International Society for Neurochemistry. This is the peer reviewed version of the following article: [Journal of Neurochemistry, 146(4):459-473, 2018], which has been published in final form at https://doi.org/10.1111/jnc.14451. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.
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資源タイプ
journal article
言語
English (英語)
ISSN
0022-3042
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eISSN
1471-4159
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関連情報
DOI
https://doi.org/10.1111/jnc.14451
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