Loss of Myh14 Increases Susceptibility to Noise-Induced Hearing Loss in CBA/CaJ Mice
MYH14 is a member of the myosin family, which has been implicated in many motile processes such as ion-channel gating, organelle translocation, and the cytoskeleton rearrangement. Mutations in MYH14 lead to a DFNA4-type hearing impairment. Further evidence also shows that MYH14 is a candidate noise-...
Veröffentlicht in: | Neural plasticity. - 1998. - 2016(2016) vom: 16., Seite 6720420 |
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1. Verfasser: | |
Weitere Verfasser: | , , , , , , , |
Format: | Online-Aufsatz |
Sprache: | English |
Veröffentlicht: |
2016
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Zugriff auf das übergeordnete Werk: | Neural plasticity |
Schlagworte: | Journal Article Research Support, Non-U.S. Gov't Myh14 protein, mouse Myosin Type II EC 3.6.1.- Myosin Heavy Chains EC 3.6.4.1 |
Zusammenfassung: | MYH14 is a member of the myosin family, which has been implicated in many motile processes such as ion-channel gating, organelle translocation, and the cytoskeleton rearrangement. Mutations in MYH14 lead to a DFNA4-type hearing impairment. Further evidence also shows that MYH14 is a candidate noise-induced hearing loss (NIHL) susceptible gene. However, the specific roles of MYH14 in auditory function and NIHL are not fully understood. In the present study, we used CRISPR/Cas9 technology to establish a Myh14 knockout mice line in CBA/CaJ background (now referred to as Myh14-/- mice) and clarify the role of MYH14 in the cochlea and NIHL. We found that Myh14-/- mice did not exhibit significant hearing loss until five months of age. In addition, Myh14-/- mice were more vulnerable to high intensity noise compared to control mice. More significant outer hair cell loss was observed in Myh14-/- mice than in wild type controls after acoustic trauma. Our findings suggest that Myh14 may play a beneficial role in the protection of the cochlea after acoustic overstimulation in CBA/CaJ mice |
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Beschreibung: | Date Completed 26.10.2017 Date Revised 13.11.2018 published: Print-Electronic Citation Status MEDLINE |
ISSN: | 1687-5443 |
DOI: | 10.1155/2016/6720420 |