Conclusion
FSCN2 mediates reduction of CDDP induced ototoxicity by inhibiting cell apoptosis.
Methods
Two-week-old Fscn2 +/+ mice and Fscn2 -/- mice were treated with two doses of cisplatin, with a 3-day recovery period in between. ABR (auditory evoked brain stem response) thresholds were measured and cochlear pathology was observed at 3 weeks of age.
Results
Both Fscn2 +/+ and Fscn2 -/- mice showed hearing loss under the effect of cisplatin, but the impairment was more severe in Fscn2 -/- mice. Further experiments showed that the percentages of outer hair cell (OHC) and spiral ganglion neuron (SGN) loss were significantly higher in cisplatin-treated Fscn2 -/- mice compared to Fscn2 +/+ mice. Additionally, knockdown of Fscn2 in HEI-OC1 cells worsened cisplatin-induced cell apoptosis.