MiR-142-3p Enhances Cell Viability and Inhibits Apoptosis by Targeting CDKN1B and TIMP3 Following Sciatic Nerve Injury

Cellular Physiology and Biochemistry

Dong-Mei Wu¹ 

关键词: MiR-142-3p;    Nerve injury;    CDKN1B;    TIMP3;    Cell cycle;    Cell apoptosis;   

DOI  :  10.1159/000489626

学科分类：分子生物学，细胞生物学和基因

来源: S Karger AG

【 摘 要 】

Background/Aims MiRNAs are involved in phenotype modulation of neural cells after peripheral nerve injury. However, the roles of miRNAs on the survival of dorsal root ganglion (DRG) neurons have not yet been fully understood. Methods In this study, the expression of miR-142-3p was measured in rat DRGs (L4-L6) during the initial 24 hours post sciatic nerve transection by microarray profiling and quantitative PCR. The functional assays including the cell viability, colony formation, cell cycle and apoptosis assays were performed in miR-142-3p mimic or inhibitor transfected cell lines. Results MiR-142-3p was identified to be siginificantly upregulated in rat DRGs (L4-L6) during the initial 24 hours post sciatic nerve transection. MiR-142-3p mimic enhanced cell viability by promoting cell cycle and inhibiting cell apoptosis in cultured DRG neurons. In addition, cyclin-dependent kinase inhibitor 1B (CDKN1B, also known as p27/Kip1) and tissue inhibitor of metalloproteinase 3 (TIMP3) were identified as targets of miR-142-3p. Furthermore, knockdown of CDKN1B or TIMP3 by specific siRNAs could reverse the effect of miR-142-3p. Conclusions In the conclusion, the results showed that miR-142-3p could promote neuronal cell cycle and inhibit apoptosis at least partially through suppressing CDKN1B and TIMP3 after peripheral nerve injury.

【 授权许可】

CC BY-NC-ND