miR-204 suppresses cochlear spiral ganglion neuron survival in vitro by targeting TMPRSS3.

Sensorineural hearing loss (SNHL) is the most common cause of hearing impairment. One of the essential steps to prevent progressive hearing loss is to protect spiral ganglion neurons (SGNs) from ongoing degeneration. MicroRNAs and TMPRSS3 (transmembrane protease, serine 3) have been reported to be involved in development of SGNs and genesis of SNHL. The aim of this study was to investigate the role of miR-204 and TMPRSS3 in SGNs. Effect of miR-204 on cell viability of SGNs was first examined using MTT (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide) assay. Expression of TMPRSS3 in SGNs with or without addition of miR-204 was assessed by real-time PCR and western blot further. A luciferase reporter activity assay was conducted to confirm target association between miR-204 and 3'-UTR of TMPRSS3. Finally, role of TMPRSS3 on cell viability of SGNs was evaluated by transfection of TMPRSS3 siRNA. Cell viability of SGNs was suppressed by miR-204 in a concentration-dependent manner. Overexpression of miR-204 reduced expression of TMPRSS3 in SGNs at both mRNA and protein levels. Binding to the 3'-UTR of TMPRSS3 by miR-204 was identified by luciferase assay. Knockdown of TMPRSS3 by siRNA significantly inhibits cell viability of SGNs. miR-204 could be a potential therapeutic target in sensorineural hearing loss.