NADPH Oxidase 3 Deficiency Protects From Noise-Induced Sensorineural Hearing Loss

The reactive oxygen species (ROS)-generating NADPH oxidase NOX3 isoform is highly and specifically expressed in the inner ear. NOX3 is needed for normal vestibular development but NOX-derived ROS have also been implicated in the pathophysiology of sensorineural hearing loss. The role of NOX-derived...
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Gespeichert in:

Autor*in:	Francis Rousset [verfasserIn] German Nacher-Soler [verfasserIn] Vivianne Beatrix Christina Kokje [verfasserIn] Stéphanie Sgroi [verfasserIn] Marta Coelho [verfasserIn] Karl-Heinz Krause [verfasserIn] Pascal Senn [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	NADPH oxidase NOX3 cochlea noise-induced hearing loss auditory neurons neuroprotection

Übergeordnetes Werk:	In: Frontiers in Cell and Developmental Biology - Frontiers Media S.A., 2014, 10(2022)
Übergeordnetes Werk:	volume:10 ; year:2022

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fcell.2022.832314

Katalog-ID:	DOAJ019845235

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520			\|a The reactive oxygen species (ROS)-generating NADPH oxidase NOX3 isoform is highly and specifically expressed in the inner ear. NOX3 is needed for normal vestibular development but NOX-derived ROS have also been implicated in the pathophysiology of sensorineural hearing loss. The role of NOX-derived ROS in noise-induced hearing loss, however, remains unclear and was addressed with the present study. Two different mouse strains, deficient in NOX3 or its critical subunit p22phox, were subjected to a single noise exposure of 2 h using an 8–16 kHz band noise at an intensity of 116–120 decibel sound pressure level. In the hours following noise exposure, there was a significant increase in cochlear mRNA expression of NOX3 in wild type animals. By using RNAscope in situ hybridization, NOX3 expression was primarily found in the Rosenthal canal area, colocalizing with auditory neurons. One day after the noise trauma, we observed a high frequency hearing loss in both knock-out mice, as well as their wild type littermates. At day seven after noise trauma however, NOX3 and p22phox knockout mice showed a significantly improved hearing recovery and a marked preservation of neurosensory cochlear structures compared to their wild type littermates. Based on these findings, an active role of NOX3 in the pathophysiology of noise-induced hearing loss can be demonstrated, in line with recent evidence obtained in other forms of acquired hearing loss. The present data demonstrates that the absence of functional NOX3 enhances the hearing recovery phase following noise trauma. This opens an interesting clinical window for pharmacological or molecular intervention aiming at post prevention of noise-induced hearing loss.
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allfieldsSound	10.3389/fcell.2022.832314 doi (DE-627)DOAJ019845235 (DE-599)DOAJf710c753abb547f2bc7d391150d33308 DE-627 ger DE-627 rakwb eng QH301-705.5 Francis Rousset verfasserin aut NADPH Oxidase 3 Deficiency Protects From Noise-Induced Sensorineural Hearing Loss 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The reactive oxygen species (ROS)-generating NADPH oxidase NOX3 isoform is highly and specifically expressed in the inner ear. NOX3 is needed for normal vestibular development but NOX-derived ROS have also been implicated in the pathophysiology of sensorineural hearing loss. The role of NOX-derived ROS in noise-induced hearing loss, however, remains unclear and was addressed with the present study. Two different mouse strains, deficient in NOX3 or its critical subunit p22phox, were subjected to a single noise exposure of 2 h using an 8–16 kHz band noise at an intensity of 116–120 decibel sound pressure level. In the hours following noise exposure, there was a significant increase in cochlear mRNA expression of NOX3 in wild type animals. By using RNAscope in situ hybridization, NOX3 expression was primarily found in the Rosenthal canal area, colocalizing with auditory neurons. One day after the noise trauma, we observed a high frequency hearing loss in both knock-out mice, as well as their wild type littermates. At day seven after noise trauma however, NOX3 and p22phox knockout mice showed a significantly improved hearing recovery and a marked preservation of neurosensory cochlear structures compared to their wild type littermates. Based on these findings, an active role of NOX3 in the pathophysiology of noise-induced hearing loss can be demonstrated, in line with recent evidence obtained in other forms of acquired hearing loss. The present data demonstrates that the absence of functional NOX3 enhances the hearing recovery phase following noise trauma. This opens an interesting clinical window for pharmacological or molecular intervention aiming at post prevention of noise-induced hearing loss. NADPH oxidase NOX3 cochlea noise-induced hearing loss auditory neurons neuroprotection Biology (General) German Nacher-Soler verfasserin aut Vivianne Beatrix Christina Kokje verfasserin aut Vivianne Beatrix Christina Kokje verfasserin aut Stéphanie Sgroi verfasserin aut Marta Coelho verfasserin aut Karl-Heinz Krause verfasserin aut Pascal Senn verfasserin aut Pascal Senn verfasserin aut In Frontiers in Cell and Developmental Biology Frontiers Media S.A., 2014 10(2022) (DE-627)770398138 (DE-600)2737824-X 2296634X nnns volume:10 year:2022 https://doi.org/10.3389/fcell.2022.832314 kostenfrei https://doaj.org/article/f710c753abb547f2bc7d391150d33308 kostenfrei https://www.frontiersin.org/articles/10.3389/fcell.2022.832314/full kostenfrei https://doaj.org/toc/2296-634X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2022
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callnumber-first	Q - Science
author	Francis Rousset
spellingShingle	Francis Rousset misc QH301-705.5 misc NADPH oxidase misc NOX3 misc cochlea misc noise-induced hearing loss misc auditory neurons misc neuroprotection misc Biology (General) NADPH Oxidase 3 Deficiency Protects From Noise-Induced Sensorineural Hearing Loss
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topic_title	QH301-705.5 NADPH Oxidase 3 Deficiency Protects From Noise-Induced Sensorineural Hearing Loss NADPH oxidase NOX3 cochlea noise-induced hearing loss auditory neurons neuroprotection
topic	misc QH301-705.5 misc NADPH oxidase misc NOX3 misc cochlea misc noise-induced hearing loss misc auditory neurons misc neuroprotection misc Biology (General)
topic_unstemmed	misc QH301-705.5 misc NADPH oxidase misc NOX3 misc cochlea misc noise-induced hearing loss misc auditory neurons misc neuroprotection misc Biology (General)
topic_browse	misc QH301-705.5 misc NADPH oxidase misc NOX3 misc cochlea misc noise-induced hearing loss misc auditory neurons misc neuroprotection misc Biology (General)
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title	NADPH Oxidase 3 Deficiency Protects From Noise-Induced Sensorineural Hearing Loss
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title_full	NADPH Oxidase 3 Deficiency Protects From Noise-Induced Sensorineural Hearing Loss
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title_sort	nadph oxidase 3 deficiency protects from noise-induced sensorineural hearing loss
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title_auth	NADPH Oxidase 3 Deficiency Protects From Noise-Induced Sensorineural Hearing Loss
abstract	The reactive oxygen species (ROS)-generating NADPH oxidase NOX3 isoform is highly and specifically expressed in the inner ear. NOX3 is needed for normal vestibular development but NOX-derived ROS have also been implicated in the pathophysiology of sensorineural hearing loss. The role of NOX-derived ROS in noise-induced hearing loss, however, remains unclear and was addressed with the present study. Two different mouse strains, deficient in NOX3 or its critical subunit p22phox, were subjected to a single noise exposure of 2 h using an 8–16 kHz band noise at an intensity of 116–120 decibel sound pressure level. In the hours following noise exposure, there was a significant increase in cochlear mRNA expression of NOX3 in wild type animals. By using RNAscope in situ hybridization, NOX3 expression was primarily found in the Rosenthal canal area, colocalizing with auditory neurons. One day after the noise trauma, we observed a high frequency hearing loss in both knock-out mice, as well as their wild type littermates. At day seven after noise trauma however, NOX3 and p22phox knockout mice showed a significantly improved hearing recovery and a marked preservation of neurosensory cochlear structures compared to their wild type littermates. Based on these findings, an active role of NOX3 in the pathophysiology of noise-induced hearing loss can be demonstrated, in line with recent evidence obtained in other forms of acquired hearing loss. The present data demonstrates that the absence of functional NOX3 enhances the hearing recovery phase following noise trauma. This opens an interesting clinical window for pharmacological or molecular intervention aiming at post prevention of noise-induced hearing loss.
abstractGer	The reactive oxygen species (ROS)-generating NADPH oxidase NOX3 isoform is highly and specifically expressed in the inner ear. NOX3 is needed for normal vestibular development but NOX-derived ROS have also been implicated in the pathophysiology of sensorineural hearing loss. The role of NOX-derived ROS in noise-induced hearing loss, however, remains unclear and was addressed with the present study. Two different mouse strains, deficient in NOX3 or its critical subunit p22phox, were subjected to a single noise exposure of 2 h using an 8–16 kHz band noise at an intensity of 116–120 decibel sound pressure level. In the hours following noise exposure, there was a significant increase in cochlear mRNA expression of NOX3 in wild type animals. By using RNAscope in situ hybridization, NOX3 expression was primarily found in the Rosenthal canal area, colocalizing with auditory neurons. One day after the noise trauma, we observed a high frequency hearing loss in both knock-out mice, as well as their wild type littermates. At day seven after noise trauma however, NOX3 and p22phox knockout mice showed a significantly improved hearing recovery and a marked preservation of neurosensory cochlear structures compared to their wild type littermates. Based on these findings, an active role of NOX3 in the pathophysiology of noise-induced hearing loss can be demonstrated, in line with recent evidence obtained in other forms of acquired hearing loss. The present data demonstrates that the absence of functional NOX3 enhances the hearing recovery phase following noise trauma. This opens an interesting clinical window for pharmacological or molecular intervention aiming at post prevention of noise-induced hearing loss.
abstract_unstemmed	The reactive oxygen species (ROS)-generating NADPH oxidase NOX3 isoform is highly and specifically expressed in the inner ear. NOX3 is needed for normal vestibular development but NOX-derived ROS have also been implicated in the pathophysiology of sensorineural hearing loss. The role of NOX-derived ROS in noise-induced hearing loss, however, remains unclear and was addressed with the present study. Two different mouse strains, deficient in NOX3 or its critical subunit p22phox, were subjected to a single noise exposure of 2 h using an 8–16 kHz band noise at an intensity of 116–120 decibel sound pressure level. In the hours following noise exposure, there was a significant increase in cochlear mRNA expression of NOX3 in wild type animals. By using RNAscope in situ hybridization, NOX3 expression was primarily found in the Rosenthal canal area, colocalizing with auditory neurons. One day after the noise trauma, we observed a high frequency hearing loss in both knock-out mice, as well as their wild type littermates. At day seven after noise trauma however, NOX3 and p22phox knockout mice showed a significantly improved hearing recovery and a marked preservation of neurosensory cochlear structures compared to their wild type littermates. Based on these findings, an active role of NOX3 in the pathophysiology of noise-induced hearing loss can be demonstrated, in line with recent evidence obtained in other forms of acquired hearing loss. The present data demonstrates that the absence of functional NOX3 enhances the hearing recovery phase following noise trauma. This opens an interesting clinical window for pharmacological or molecular intervention aiming at post prevention of noise-induced hearing loss.
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title_short	NADPH Oxidase 3 Deficiency Protects From Noise-Induced Sensorineural Hearing Loss
url	https://doi.org/10.3389/fcell.2022.832314 https://doaj.org/article/f710c753abb547f2bc7d391150d33308 https://www.frontiersin.org/articles/10.3389/fcell.2022.832314/full https://doaj.org/toc/2296-634X
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up_date	2024-07-04T01:10:29.954Z
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At day seven after noise trauma however, NOX3 and p22phox knockout mice showed a significantly improved hearing recovery and a marked preservation of neurosensory cochlear structures compared to their wild type littermates. Based on these findings, an active role of NOX3 in the pathophysiology of noise-induced hearing loss can be demonstrated, in line with recent evidence obtained in other forms of acquired hearing loss. The present data demonstrates that the absence of functional NOX3 enhances the hearing recovery phase following noise trauma. 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NADPH Oxidase 3 Deficiency Protects From Noise-Induced Sensorineural Hearing Loss

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