南京大学高下等研究人员合作发现，条件性Tnfaip6基因敲除在内耳毛细胞中不改变听觉功能。2024年12月17日，国际知名学术期刊《神经科学通报》发表了这一成果。

研究人员表示，噪声性听力损失是全球公共卫生问题，其特点是听力敏感度的暂时性或永久性变化。这种情况与炎症反应密切相关，靶向炎症基因肿瘤坏死因子-α（TNFα）的干预已知可以减轻耳蜗噪声损伤。TNFα诱导蛋白（TNFAIPs）是一类半透明的酸性蛋白，TNFAIP6与炎症反应有显著关联。至今，关于TNFAIP6在内耳中的水平的报道较少。

为了阐明具体机制，研究人员生成了条件性Tnfaip6敲除（Tnfaip6 cKO）的小鼠模型。对毛细胞形态和功能的评估显示，Tnfaip6 cKO小鼠与野生型小鼠之间在毛细胞数量或带状突触上没有显著差异。此外，在噪音环境下，毛细胞数量或听力功能也没有显著变化。这些结果表明，Tnfaip6对听觉系统没有显著影响。

附：英文原文

Title: Conditional Tnfaip6-Knockout in Inner Ear Hair Cells Does not Alter Auditory Function

Author: Qiu, Yue, Gao, Song, Ding, Xiaoqiong, Lu, Jie, Ji, Xinya, Hao, Wenli, Cheng, Siqi, Du, Haolinag, Gu, Yajun, Yu, Chenjie, Cheng, Cheng, Gao, Xia

Issue&Volume: 2024-12-17

Abstract: Noise-induced hearing loss is a worldwide public health issue that is characterized by temporary or permanent changes in hearing sensitivity. This condition is closely linked to inflammatory responses, and interventions targeting the inflammatory gene tumor necrosis factor-alpha (TNFα) are known to mitigate cochlear noise damage. TNFα-induced proteins (TNFAIPs) are a family of translucent acidic proteins, and TNFAIP6 has a notable association with inflammatory responses. To date, there have been few reports on TNFAIP6 levels in the inner ear. To elucidate the precise mechanism, we generated transgenic mouse models with conditional knockout of Tnfaip6 (Tnfaip6 cKO). Evaluation of hair cell morphology and function revealed no significant differences in hair cell numbers or ribbon synapses between Tnfaip6 cKO and wild-type mice. Moreover, there were no notable variations in hair cell numbers or hearing function in noisy environments. Our results indicate that Tnfaip6 does not have a substantial impact on the auditory system.

DOI: 10.1007/s12264-024-01326-8

Source: https://link.springer.com/article/10.1007/s12264-024-01326-8