感音神经性聋是最常见的听觉残疾，内耳毛细胞的突触病变是其发生的重要病理机制。研究表明Dynamin蛋白是维持突触囊泡内吞的关键蛋白，但其调控机制并不清楚。我们发现miRNA具有调节突触蛋白表达的功能，前期实验结果提示miRNA30b/140能够同时调控Dynamin蛋白的表达，且两者具有正向协调作用，但miRNA30b和miRNA140之间通过什么方式进行沟通并不清楚。结合前期基础我们推测：多个miRNA可调控Dynamin蛋白，lncRNA-Malat1可能介导miR-30b和miR-140之间的信号沟通，作为两个miR的ceRNA参与Dynamin蛋白的调控。为验证这一假说，本项目拟运用蛋白组学、电生理学等多种手段，通过生理、病理模型来证实“lncRNA-Malat1-miR-蛋白-内吞假说”。通过本研究可望完善听信号突触传递的生理机制，从囊泡内吞回收层面阐释感音神经性聋可能发病原因。

Sensorineural hearing loss(SNHL)is one of the most common reason of auditory sense disability.Synapse pathological change of inner hair cells is an important pathological mechanism of it .Studies have shown that Dynamin is the key protein to maintain synaptic vesicle endocytosis but how to regulate is not clear.We found that miRNAs have the function of regulating synaptic protein expression,and previous study results indicated that miRNA30b/140 can regulate the expression of Dynamin protein at the same time both of them have a positive coordination effect.However it is not known how miRNA30b and miRNA140 to communicate with each other.Combined with the previous foundation, we infer that lncRNA-Malat1 may be involved in the interaction between miR-30b and miR-140,it affects the process of vesicles endocytosis of hair cells, as the act of ceRNA of the two miRs participates in the regulation of Dynamin.To verify this ,our project intends to use a variety of means, such as proteomics , electrophysiology, etc .To confirm“lncRNA-Malat1-miR-protein-endocytosis hypothesis”by a physiological and pathological model.Through this study, we hope to improve the physiological mechanism of auditory synaptic transmission.Explain the possible. pathogenesis of Sensorineural hearing loss from the perspective of vesicle endocytosis.