• Lili Zhao, Ying Yuan, Ping Li, Jiacheng Pan, Jing Qin, Yisheng Liu, Yu Zhang, Feng Tian, Bin Yu, and Songlin Zhou.
• Key laboratory of neuroregeneration of Jiangsu and Ministry of Education, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, Jiangsu 226001, China; State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing Biomedical Research Institute, Nanjing University, Nanjing, Jiangsu 210000, China.
• Neuroscience. 2018 May 21; 379: 239-245.

AbstractFollowing peripheral nerve injury, Schwann Cells (SCs) undergo dedifferentiation, proliferation, migration, and remyelination. Recent works demonstrated the importance of the short non-coding RNA (miRNAs) in SC dedifferentiation and remyelination after nerve injury. Previously, we found some miRNAs like miR-9, miR-221, miR-222 and miR-182 could regulate the proliferation and migration of SCs. Therefore, it is imperative to ask whether these miRNAs could regulate the myelination of SCs. Here we demonstrated that miR-221-3p could inhibit the myelination of SCs when co-cultured with dorsal root ganglion cells in vitro. In addition, NGF1-A binding protein 1 (Nab1) which was essential for SCs myelination could be downregulated by miR-221-3p. Suppressing the expression of Nab1 could reverse the promotion of miR-221-3p antagomir on SC myelination. The effects of miR-221-3p on SC myelination might be used to improve peripheral nerve regeneration, thus offering a new approach to peripheral nerve repair.Copyright © 2018 IBRO. All rights reserved.

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