LncRNA TNXA-PS1 modulates Schwann cells by functioning as a competing endogenous RNA following nerve injury

As a major glia in peripheral nerve system, Schwann cells play a critical role in peripheral nerve injury repair. Searching efficient approach to promote Schwann cell activation might facilitate peripheral nerve repair. Long noncoding RNAs (lncRNAs) have been shown to regulate gene expression and take part in many biological processes. However, the role of lncRNAs in peripheral nerve regeneration is not fully understood. In this study, we obtained a global lncRNA portrayal following sciatic nerve injury in male rats using microarray and further investigated one of these dys-regulated lncRNAs, TNXA-PS1, confirming its vital role in regulating Schwann cells. Silencing TNAX-PS1 could promote Schwann cell migration, and mechanism analyses showed that TNXA-PS1 might exert its regulatory role by sponging miR-24-3p/miR-152-3p and affecting Dusp1 expression. Collectively, we obtained a systematic lncRNA expression profiling of sciatic nerve segments following nerve injury in rats and suggested lncRNA TNXA-PS1 as a key regulator of Schwann cell migration, providing a potential therapeutic target for nerve injury repair. Significance Statement Peripheral nervous system has an intrinsic regeneration capacity after injury, during which Schwann cells play a crucial role in. Thus, further exploration of functional molecules in Schwann cell phenotype modulation is of great importance. We have identified a set of dys-regulated lncRNAs in rats following sciatic nerve injury and found that the expression of TNXA-PS1 was significantly down-regulated. Mechanically analyses showed that TNXA-PS1 might act as a competing endogenous RNA to affect Dusp1 expression, regulating migration of Schwann cells. This study provides a global landscape of lncRNAs following sciatic nerve injury in rats for the first time and broadens the function of lncRNA during nerve injury. The investigation of TNXA-PS1 might facilitate the development of novel targets for nerve injury therapy.