Cochlin Deficiency Protects Aged Mice from Noise-Induced Hearing Loss

Several studies have shown that type IV fibrocytes, located in the spiral ligament, degenerate first after noise exposure. Interestingly, this is the region where <i>Coch</i> expression is most abundant. As it is suggested that cochlin plays a role in our innate immune system, our goal i...

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Autores principales: Dorien Verdoodt, Noa Peeleman, Krystyna Szewczyk, Guy Van Camp, Peter Ponsaerts, Vincent Van Rompaey
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Publicado: MDPI AG 2021
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Acceso en línea:https://doaj.org/article/ebb5cd1cf8f14c7db193894653ccae22
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spelling oai:doaj.org-article:ebb5cd1cf8f14c7db193894653ccae222021-11-11T17:01:26ZCochlin Deficiency Protects Aged Mice from Noise-Induced Hearing Loss10.3390/ijms2221115491422-00671661-6596https://doaj.org/article/ebb5cd1cf8f14c7db193894653ccae222021-10-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/21/11549https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067Several studies have shown that type IV fibrocytes, located in the spiral ligament, degenerate first after noise exposure. Interestingly, this is the region where <i>Coch</i> expression is most abundant. As it is suggested that cochlin plays a role in our innate immune system, our goal is to investigate hearing thresholds and inner ear inflammation after noise exposure in <i>Coch</i> knockout (<i>Coch<sup>−/−</sup></i>) mice compared to <i>Coch</i> wildtype (<i>Coch<sup>+/+</sup></i>) mice. Animals were randomly allocated to a noise exposure group and a control group. Vestibular and auditory testing was performed at 48 h and one week after noise exposure. Whole mount staining and cryosectioning of the cochlea was performed in order to investigate hair cells, spiral ganglion neurons, inner ear inflammation, <i>Coch</i> expression and fibrocyte degeneration. Hearing assessment revealed that <i>Coch<sup>+/+</sup></i> mice had significantly larger threshold shifts than <i>Coch<sup>−/−</sup></i> mice after noise exposure. We were unable to identify any differences in hair cells, neurons, fibrocytes and influx of macrophages in the inner ear between both groups. Interestingly, <i>Coch</i> expression was significantly lower in the group exposed to noise. Our results indicate that the absence of <i>Coch</i> has a protective influence on hearing thresholds after noise exposure, but this is not related to reduced inner ear inflammation in the knockout.Dorien VerdoodtNoa PeelemanKrystyna SzewczykGuy Van CampPeter PonsaertsVincent Van RompaeyMDPI AGarticlenoise exposureinner ear inflammation<i>Coch</i> knockoutspiral ligamentBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 11549, p 11549 (2021)
institution DOAJ
collection DOAJ
language EN
topic noise exposure
inner ear inflammation
<i>Coch</i> knockout
spiral ligament
Biology (General)
QH301-705.5
Chemistry
QD1-999
spellingShingle noise exposure
inner ear inflammation
<i>Coch</i> knockout
spiral ligament
Biology (General)
QH301-705.5
Chemistry
QD1-999
Dorien Verdoodt
Noa Peeleman
Krystyna Szewczyk
Guy Van Camp
Peter Ponsaerts
Vincent Van Rompaey
Cochlin Deficiency Protects Aged Mice from Noise-Induced Hearing Loss
description Several studies have shown that type IV fibrocytes, located in the spiral ligament, degenerate first after noise exposure. Interestingly, this is the region where <i>Coch</i> expression is most abundant. As it is suggested that cochlin plays a role in our innate immune system, our goal is to investigate hearing thresholds and inner ear inflammation after noise exposure in <i>Coch</i> knockout (<i>Coch<sup>−/−</sup></i>) mice compared to <i>Coch</i> wildtype (<i>Coch<sup>+/+</sup></i>) mice. Animals were randomly allocated to a noise exposure group and a control group. Vestibular and auditory testing was performed at 48 h and one week after noise exposure. Whole mount staining and cryosectioning of the cochlea was performed in order to investigate hair cells, spiral ganglion neurons, inner ear inflammation, <i>Coch</i> expression and fibrocyte degeneration. Hearing assessment revealed that <i>Coch<sup>+/+</sup></i> mice had significantly larger threshold shifts than <i>Coch<sup>−/−</sup></i> mice after noise exposure. We were unable to identify any differences in hair cells, neurons, fibrocytes and influx of macrophages in the inner ear between both groups. Interestingly, <i>Coch</i> expression was significantly lower in the group exposed to noise. Our results indicate that the absence of <i>Coch</i> has a protective influence on hearing thresholds after noise exposure, but this is not related to reduced inner ear inflammation in the knockout.
format article
author Dorien Verdoodt
Noa Peeleman
Krystyna Szewczyk
Guy Van Camp
Peter Ponsaerts
Vincent Van Rompaey
author_facet Dorien Verdoodt
Noa Peeleman
Krystyna Szewczyk
Guy Van Camp
Peter Ponsaerts
Vincent Van Rompaey
author_sort Dorien Verdoodt
title Cochlin Deficiency Protects Aged Mice from Noise-Induced Hearing Loss
title_short Cochlin Deficiency Protects Aged Mice from Noise-Induced Hearing Loss
title_full Cochlin Deficiency Protects Aged Mice from Noise-Induced Hearing Loss
title_fullStr Cochlin Deficiency Protects Aged Mice from Noise-Induced Hearing Loss
title_full_unstemmed Cochlin Deficiency Protects Aged Mice from Noise-Induced Hearing Loss
title_sort cochlin deficiency protects aged mice from noise-induced hearing loss
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/ebb5cd1cf8f14c7db193894653ccae22
work_keys_str_mv AT dorienverdoodt cochlindeficiencyprotectsagedmicefromnoiseinducedhearingloss
AT noapeeleman cochlindeficiencyprotectsagedmicefromnoiseinducedhearingloss
AT krystynaszewczyk cochlindeficiencyprotectsagedmicefromnoiseinducedhearingloss
AT guyvancamp cochlindeficiencyprotectsagedmicefromnoiseinducedhearingloss
AT peterponsaerts cochlindeficiencyprotectsagedmicefromnoiseinducedhearingloss
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