ENT institute and Department of Otorhinolaryngology, Eye & ENT Hospital, Fudan University, 83 Fenyang Road, Shanghai, 200031, China.
NHC Key Laboratory of Hearing Medicine (Fudan University), Shanghai, 200031, China.
Cell Biol Toxicol. 2021 Oct;37(5):751-771. doi: 10.1007/s10565-021-09596-y. Epub 2021 Mar 15.
Noise-induced hearing loss represents a commonly diagnosed type of hearing disability, severely impacting the quality of life of individuals. The current work is aimed at assessing the effects of DNA methylation on noise-induced hearing loss.
Blocking DNA methyltransferase 1 (DNMT1) activity with a selective inhibitor RG108 or silencing DNMT1 with siRNA was used in this study. Auditory brainstem responses were measured at baseline and 2 days after trauma in mice to assess auditory functions. Whole-mount immunofluorescent staining and confocal microcopy of mouse inner ear specimens were performed to analyze noise-induced damage in cochleae and the auditory nerve at 2 days after noise exposure.
The results showed that noise exposure caused threshold elevation of auditory brainstem responses and cochlear hair cell loss. Whole-mount cochlea staining revealed a reduction in the density of auditory ribbon synapses between inner hair cells and spiral ganglion neurons. Inhibition of DNA methyltransferase activity via a non-nucleoside specific pharmacological inhibitor, RG108, or silencing of DNA methyltransferase-1 with siRNA significantly attenuated ABR threshold elevation, hair cell damage, and the loss of auditory synapses.
This study suggests that inhibition of DNMT1 ameliorates noise-induced hearing loss and indicates that DNMT1 may be a promising therapeutic target. Graphical Headlights • RG108 protected against noise-induced hearing loss • RG108 administration protected against noise-induced hair cell loss and auditory neural damage. • RG108 administration attenuated oxidative stress-induced DNA damage and subsequent apoptosis-mediated cell loss in the cochlea after noise exposure.
噪声性听力损失是一种常见的听力障碍类型,严重影响个体的生活质量。本研究旨在评估 DNA 甲基化对噪声性听力损失的影响。
本研究采用选择性 DNA 甲基转移酶 1(DNMT1)抑制剂 RG108 或 siRNA 沉默 DNMT1。在创伤后 2 天,通过测量小鼠听觉脑干反应来评估听觉功能。对小鼠内耳标本进行全耳蜗免疫荧光染色和共聚焦显微镜检查,以分析噪声暴露后 2 天耳蜗和听神经的损伤情况。
结果表明,噪声暴露导致听觉脑干反应阈值升高和耳蜗毛细胞损失。全耳蜗染色显示内毛细胞和螺旋神经节神经元之间的听觉带状突触密度降低。通过非核苷特异性药理抑制剂 RG108 抑制 DNA 甲基转移酶活性或用 siRNA 沉默 DNA 甲基转移酶-1,可显著减轻 ABR 阈值升高、毛细胞损伤和听觉突触丧失。
本研究表明抑制 DNMT1 可改善噪声性听力损失,并表明 DNMT1 可能是一个有前途的治疗靶点。
图注亮点 • RG108 可预防噪声性听力损失 • RG108 治疗可预防噪声诱导的毛细胞损失和听神经损伤。 • RG108 治疗可减轻噪声暴露后耳蜗中氧化应激诱导的 DNA 损伤和随后的细胞凋亡。