Deletion of Oncomodulin Gives Rise to Early Progressive Cochlear Dysfunction in C57 and CBA Mice

Ca2+ signaling is a major contributor to sensory hair cell function in the cochlea. Oncomodulin (OCM) is a Ca2+ binding protein (CaBP) preferentially expressed in outer hair cells (OHCs) of the cochlea and few other specialized cell types. Here, we expand on our previous reports and show that OCM de...

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Autores principales:	Leslie K. Climer, Aubrey J. Hornak, Kaitlin Murtha, Yang Yang, Andrew M. Cox, Preston L. Simpson, Andy Le, Dwayne D. Simmons
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	oncomodulin efferent hearing loss Ca2+ buffer knockout mice hair cells Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571
Acceso en línea:	https://doaj.org/article/5f4612aa05074961beecf0eb0bd2d733
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spelling	oai:doaj.org-article:5f4612aa05074961beecf0eb0bd2d7332021-11-15T13:58:35ZDeletion of Oncomodulin Gives Rise to Early Progressive Cochlear Dysfunction in C57 and CBA Mice1663-436510.3389/fnagi.2021.749729https://doaj.org/article/5f4612aa05074961beecf0eb0bd2d7332021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fnagi.2021.749729/fullhttps://doaj.org/toc/1663-4365Ca2+ signaling is a major contributor to sensory hair cell function in the cochlea. Oncomodulin (OCM) is a Ca2+ binding protein (CaBP) preferentially expressed in outer hair cells (OHCs) of the cochlea and few other specialized cell types. Here, we expand on our previous reports and show that OCM delays hearing loss in mice of two different genetic backgrounds: CBA/CaJ and C57Bl/6J. In both backgrounds, genetic disruption of Ocm leads to early progressive hearing loss as measured by auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE). In both strains, loss of Ocm reduced hearing across lifetime (hearing span) by more than 50% relative to wild type (WT). Even though the two WT strains have very different hearing spans, OCM plays a considerable and similar role within their genetic environment to regulate hearing function. The accelerated age-related hearing loss (ARHL) of the Ocm KO illustrates the importance of Ca2+ signaling in maintaining hearing health. Manipulation of OCM and Ca2+ signaling may reveal important clues to the systems of function/dysfunction that lead to ARHL.Leslie K. ClimerAubrey J. HornakKaitlin MurthaYang YangAndrew M. CoxPreston L. SimpsonAndy LeDwayne D. SimmonsDwayne D. SimmonsFrontiers Media S.A.articleoncomodulinefferenthearing lossCa2+ bufferknockout micehair cellsNeurosciences. Biological psychiatry. NeuropsychiatryRC321-571ENFrontiers in Aging Neuroscience, Vol 13 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	oncomodulin efferent hearing loss Ca2+ buffer knockout mice hair cells Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571
spellingShingle	oncomodulin efferent hearing loss Ca2+ buffer knockout mice hair cells Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Leslie K. Climer Aubrey J. Hornak Kaitlin Murtha Yang Yang Andrew M. Cox Preston L. Simpson Andy Le Dwayne D. Simmons Dwayne D. Simmons Deletion of Oncomodulin Gives Rise to Early Progressive Cochlear Dysfunction in C57 and CBA Mice
description	Ca2+ signaling is a major contributor to sensory hair cell function in the cochlea. Oncomodulin (OCM) is a Ca2+ binding protein (CaBP) preferentially expressed in outer hair cells (OHCs) of the cochlea and few other specialized cell types. Here, we expand on our previous reports and show that OCM delays hearing loss in mice of two different genetic backgrounds: CBA/CaJ and C57Bl/6J. In both backgrounds, genetic disruption of Ocm leads to early progressive hearing loss as measured by auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE). In both strains, loss of Ocm reduced hearing across lifetime (hearing span) by more than 50% relative to wild type (WT). Even though the two WT strains have very different hearing spans, OCM plays a considerable and similar role within their genetic environment to regulate hearing function. The accelerated age-related hearing loss (ARHL) of the Ocm KO illustrates the importance of Ca2+ signaling in maintaining hearing health. Manipulation of OCM and Ca2+ signaling may reveal important clues to the systems of function/dysfunction that lead to ARHL.
format	article
author	Leslie K. Climer Aubrey J. Hornak Kaitlin Murtha Yang Yang Andrew M. Cox Preston L. Simpson Andy Le Dwayne D. Simmons Dwayne D. Simmons
author_facet	Leslie K. Climer Aubrey J. Hornak Kaitlin Murtha Yang Yang Andrew M. Cox Preston L. Simpson Andy Le Dwayne D. Simmons Dwayne D. Simmons
author_sort	Leslie K. Climer
title	Deletion of Oncomodulin Gives Rise to Early Progressive Cochlear Dysfunction in C57 and CBA Mice
title_short	Deletion of Oncomodulin Gives Rise to Early Progressive Cochlear Dysfunction in C57 and CBA Mice
title_full	Deletion of Oncomodulin Gives Rise to Early Progressive Cochlear Dysfunction in C57 and CBA Mice
title_fullStr	Deletion of Oncomodulin Gives Rise to Early Progressive Cochlear Dysfunction in C57 and CBA Mice
title_full_unstemmed	Deletion of Oncomodulin Gives Rise to Early Progressive Cochlear Dysfunction in C57 and CBA Mice
title_sort	deletion of oncomodulin gives rise to early progressive cochlear dysfunction in c57 and cba mice
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/5f4612aa05074961beecf0eb0bd2d733
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Deletion of Oncomodulin Gives Rise to Early Progressive Cochlear Dysfunction in C57 and CBA Mice

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