Yue Qiu1 · Song Gao1 · Xiaoqiong Ding2 · Jie Lu3 · Xinya Ji3 · Wenli Hao1 · Siqi Cheng1 · Haolinag Du1 · Yajun Gu1 · Chenjie Yu1,4 · Cheng Cheng1,4 · Xia Gao1,41 Department of Otolaryngology-Head and Neck Surgery, Jiangsu Provincial Key Medical Discipline (Laboratory), Nanjing Drum Tower Hospital, The Afliated Hospital of Nanjing University Medical School, Nanjing 210008, China
2 Department of Otolaryngology-Head and Neck Surgery, Zhongda Hospital, Southeast University, Nanjing 210008, China
3 Northern Jiangsu People’s Hospital Afliated to Yangzhou University, Yangzhou 225001, China
4 Research Institute of Otolaryngology, Nanjing 210008, China
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.
Keywords
Noise; Tnfaip6; Hair cells; Hearing loss
