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: | , , , , , |
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| Formato: | article |
| Lenguaje: | EN |
| Publicado: |
MDPI AG
2021
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| Materias: | |
| Acceso en línea: | https://doaj.org/article/ebb5cd1cf8f14c7db193894653ccae22 |
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| Sumario: | 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. |
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