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FGF22 protects hearing function from gentamycin ototoxicity by maintaining ribbon synapse number
Shuna Li1, Lihua Hang2, Yongming Ma1
1Department of Otolaryngology and Head-Neck Surgery, Zhenjiang First People's Hospital, the Affiliated People's Hospital of Jiangsu University, 8 Dianli Rd, Zhenjiang, Jiangsu, 212000, China.
Hearing Research
|December 8, 2015
Summary
Fibroblast growth factor 22 (FGF22) protects inner hair cell ribbon synapses from gentamicin-induced hearing loss. FGF22 maintains synapse number, likely by inhibiting MEF2D, offering a potential therapeutic strategy.
Area of Science:
- Ototolaryngology
- Neuroscience
- Molecular Biology
Background:
- Inner hair cell (IHC) ribbon synapses are crucial for auditory signal transmission.
- These synapses are vulnerable to ototoxicity, but the mechanisms of damage are unclear.
- Fibroblast growth factor 22 (FGF22) is implicated in synapse formation.
Purpose of the Study:
- To investigate the role of FGF22 in protecting cochlear ribbon synapses against gentamicin-induced ototoxicity.
- To explore the underlying molecular mechanisms involving myocyte enhancer factor 2D (MEF2D).
Main Methods:
- Gentamicin was administered to mice to induce ototoxicity.
- Ribbon synapse numbers were quantified using immunostaining (GluR2&3/CtBP2).
- Gene expression (FGF22, MEF2D) was analyzed via RT-PCR; protein localization via immunostaining.
- Hearing function was assessed using auditory brainstem responses (ABRs).
Main Results:
- Gentamicin reduced ribbon synapse numbers and caused hearing impairment without affecting hair cells.
- FGF22 protein was localized to IHCs; gentamicin decreased FGF22 and increased MEF2D expression.
- Recombinant FGF22 administration inhibited MEF2D, preserved ribbon synapses, and restored hearing.
Conclusions:
- FGF22 plays a protective role against gentamicin-induced ototoxicity in cochlear IHC ribbon synapses.
- FGF22 may restore hearing loss by maintaining synapse number, potentially through MEF2D inhibition.
- Targeting FGF22 could be a therapeutic strategy for hearing loss caused by ototoxicity.
