Objective: Sensorineural hearing loss (SNHL) is caused by damage to hair cells followed by degeneration of the spiral ganglion neurons (SGNs), and cochlear implanting is an effective treatment. Unfortunately, the progressive hearing loss is still found due to ongoing degeneration of cochlear SGNs. The aim of this study was to investigate the neuroprotective effect of anti-miR204 on SGNs in vivo.
Methods: Our recent in vitro work suggested that anti-miR204 could be a potential therapeutic strategy in SNHL via rescue cochlear SGNs. In order to further our knowledge of miR204 on SGNs in vivo, we made a kanamycin ototoxicity model and then virus containing the anti-miR204 gene (AAV1-anti-miR204) was microinjected into the cochlear of the model to monitor the effect.
Results: The SGNs were rescued by anti-miR204 in the kanamycin ototoxicity mouse group compared to the sham group. Moreover, expression of TMPRSS3 in SGNs was saved by anti-miR204 treatment.
Conclusion: Anti-miR204 might be an alternate way to alleviate the degeneration of cochlear SGNs of kanamycin ototoxicity mice.
Keywords: Kanamycin ototoxicity; MiR204; sensorineural hearing loss; spiral ganglion neurons TMPRSS3.