Nox3-Derived Superoxide in Cochleae Induces Sensorineural Hearing Loss

• DOI: 10.1523/jneurosci.2672-20.2021
• Publication Date: 2021-04-13T18:12:48Z
• Authors: Hiroaki Mohri; Yuzuru Ninoyu; Hirofumi Sakaguchi; Shigeru Hirano; Naoaki Saito; Takehiko Ueyama
• Keywords: Spiral ganglion

Reactive oxygen species (ROS) produced by NADPH oxidases (Nox) contribute to the development of different types sensorineural hearing loss (SNHL), a common impairment in humans with no established treatment. Although essential role Nox3 otoconia biosynthesis and its possible involvement have been reported rodents, immunohistological methods targeted at detecting expression inner ear cells reveal ambiguous results. Therefore, mechanism underlying Nox3-dependent SNHL remains unclear warrants further investigation. We generated Nox3-Cre knock-in mice, which was replaced Cre recombinase ( ). Using Nox3-Cre;tdTomato mice either sex, tdTomato is expressed under control promoter, we determined Nox3-expressing regions cell ear. cochlea included various supporting cells, outer hair spiral ganglion neurons. increased cisplatin, age, noise insults. Moreover, especially basal turn cochlea, played roles ROS-related SNHL. The extent follows following order: cisplatin-induced > age-related noise-induced loss. Here, on basis , can be used as reporter system +/− ;tdTomato +/+ ), -KO ) demonstrate that inhibition promising strategy for SNHL, such HL, HL. SIGNIFICANCE STATEMENT found ear, using this study. insults specific resulted (apoptosis) cells. Thus, might serve molecular target therapeutics loss, particularly cisplatin-induced, age-related,