周围神经损伤是严重危害人类健康的疾病之一，治愈这一疾病的核心问题是揭示周围神经损伤后的再生机制。竞争性内源RNA（ceRNA）是近几年来提出的转录后调控新机制，其核心内容是：具有相同 miRNA 应答元件的转录产物可以通过竞争性的结合相同miRNA来影响对方的表达水平，从而调控相应的生物学功能。本课题组的前期研究和最新的文献资料显示：LncRNA- NONMMUG014387可能作为ceRNA竞争性的结合Mir-9从而影响Cthrc1的表达，并进而影响雪旺细胞的生物活性以及损伤后周围神经的再生能力。本项目将综合利用分子生物学、细胞生物学、组织工程学等手段，分别从体外和体内两个方面来验证NONMMUG014387、Mir-9和Cthrc1三者之间的调控关系以及这种调控作用对雪旺细胞生物活性和周围神经再生能力的影响。进一步阐释损伤后周围神经再生的分子机制，为修复周围神经损伤提供新的途径。

Peripheral nerve injury is a common clinical problem that greatly compromises a patient’s quality of life. The key problem in curing this disease is to elucidate the molecular-biological mechanisms underlying peripheral nerve regeneration. According to the competitive endogenous RNA (ceRNA) hypothesis, lncRNA and mRNA may share the same microRNA response element to regulate each other by competitively binding to microRNA. In a previous study, we observe that LncRNA-NONMMUG014387 and Cthrc1 can both combine with Mir-9. Mir-9 expression is down-regulated in schwann cells overexpressing lncRNA-NONMMUG014387 and is associated with peripheral nerve regeneration. We presume that lncRNA- NONMMUG014387 and Cthrc1 could act as competing endogenous RNAs to affect the function of schwann cells and peripheral nerve regeneration. Based on our previous published results, we plan to measure the ceRNA mechanism and the effect on schwann cells and peripheral nerve regeneration by Molecular biology, cell biology, tissue engineering, neuroelectrophysiology technique. Our study will provide a new understanding of nerve regeneration and a potential mechanism for repairing peripheral nerve injury.