The proliferation and migration of Schwann cells contribute to nerve regeneration after peripheral nerve injury (PNI). In recent years, roles of long non-coding RNAs (lncRNAs) in PNI have been gradually uncovered. However, a highly conserved nuclear lncRNA Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in peripheral nerve regeneration remains enigmatic. MALAT1 expression in injured sciatic nerve of mice with PNI was measured by real-time PCR. The proliferative and migrative abilities of Schwann cells were determined after upregulating or downregulating Malat1. The relationship among MALAT1, miR-129-5p, and BDNF was measured. In this study, we found elevated MALAT1 expression in injured sciatic nerve. MALAT1 upregulation in Schwann cells promoted cell proliferation and migration. However, downregulation of MALAT1 caused the suppression of Schwann cell proliferation and migration. Mechanistically, we discovered MALAT1 negatively regulated miR-129-5p through directly binding. Brain-derived neurotrophic factor (BDNF) was a target of miR-129-5p. MALAT1 positively modulated BDNF expression and secretion via decreasing miR-129-5p. Downregulation of BDNF rescued the influences of MALAT1 overexpression on Schwann cell proliferation and migration. In conclusion, MALAT1 was enhanced after PNI and it promoted the proliferation and migration of Schwann cells through sponging miR-129-5p to increase BDNF expression and secretion. This study proved that MALAT1 may be a vital regulator in peripheral nerve regeneration.

雪旺细胞的增殖和迁移有助于周围神经损伤（PNI）后的神经再生。近年来，长非编码RNA（lncRNA）在PNI中的作用已逐渐被发现。但是，在周围神经再生中高度保守的核lncRNA转移相关的肺腺癌转录本1（MALAT1）仍然是个谜。通过实时PCR测量PNI小鼠受损的坐骨神经中MALAT1的表达。在上调或下调Malat1后确定雪旺细胞的增殖和迁移能力。测量了MALAT1，miR-129-5p和BDNF之间的关系。在这项研究中，我们发现受损的坐骨神经中MALAT1表达升高。雪旺细胞中的MALAT1上调促进细胞增殖和迁移。然而，MALAT1的下调引起了雪旺氏细胞增殖和迁移的抑制。从机理上讲，我们发现MALAT1通过直接结合而负调控miR-129-5p。脑源性神经营养因子（BDNF）是miR-129-5p的靶标。MALAT1通过降低miR-129-5p积极调节BDNF的表达和分泌。BDNF的下调挽救了MALAT1过表达对雪旺细胞增殖和迁移的影响。总之，MALAT1在PNI后得到增强，并通过海绵化miR-129-5p促进BDNF的表达和分泌，促进了雪旺细胞的增殖和迁移。这项研究证明，MALAT1可能是周围神经再生的重要调节剂。我们发现MALAT1通过直接结合负调控miR-129-5p。脑源性神经营养因子（BDNF）是miR-129-5p的靶标。MALAT1通过降低miR-129-5p积极调节BDNF的表达和分泌。BDNF的下调挽救了MALAT1过表达对雪旺细胞增殖和迁移的影响。总之，MALAT1在PNI后得到增强，并通过海绵化miR-129-5p促进BDNF的表达和分泌，促进了雪旺细胞的增殖和迁移。这项研究证明MALAT1可能是周围神经再生的重要调节剂。我们发现MALAT1通过直接结合负调控miR-129-5p。脑源性神经营养因子（BDNF）是miR-129-5p的靶标。MALAT1通过降低miR-129-5p积极调节BDNF的表达和分泌。BDNF的下调挽救了MALAT1过表达对雪旺细胞增殖和迁移的影响。总之，MALAT1在PNI后得到增强，并通过海绵化miR-129-5p促进BDNF的表达和分泌，促进了雪旺细胞的增殖和迁移。这项研究证明MALAT1可能是周围神经再生的重要调节剂。BDNF的下调挽救了MALAT1过表达对雪旺细胞增殖和迁移的影响。总之，MALAT1在PNI后得到增强，并通过海绵化miR-129-5p促进BDNF的表达和分泌，促进了雪旺细胞的增殖和迁移。这项研究证明MALAT1可能是周围神经再生的重要调节剂。BDNF的下调挽救了MALAT1过表达对雪旺细胞增殖和迁移的影响。总之，MALAT1在PNI后得到增强，并通过海绵化miR-129-5p促进BDNF的表达和分泌，促进了雪旺细胞的增殖和迁移。这项研究证明MALAT1可能是周围神经再生的重要调节剂。