Cochlin Deficiency Protects Aged Mice from Noise-Induced Hearing Loss
2021
Dorien Verdoodt | Noa Peeleman | Krystyna Szewczyk | Guy Van Camp | Peter Ponsaerts | Vincent Van Rompaey
Several studies have shown that type IV fibrocytes, located in the spiral ligament, degenerate first after noise exposure. Interestingly, this is the region where Coch 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 Coch knockout (Coch<sup>−/−</sup>) mice compared to Coch wildtype (Coch<sup>+/+</sup>) 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, Coch expression and fibrocyte degeneration. Hearing assessment revealed that Coch<sup>+/+</sup> mice had significantly larger threshold shifts than Coch<sup>−/−</sup> 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, Coch expression was significantly lower in the group exposed to noise. Our results indicate that the absence of Coch 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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