MicroRNA-409 promotes recovery of spinal cord injury by regulating ZNF366.

OBJECTIVE: To explore the role of microRNA-409 in spinal cord injury (SCI) recovery and its underlying mechanism. MATERIALS AND METHODS: The mouse SCI model was first established, and the difference in recovery of grip strength was detected. MicroRNA-409 expressions in mice tissues from sham operation group and SCI group were detected by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR). We further increased microRNA-409 level in mice spinal cord by plasmids transfection. Luciferase activity was detected to verify the direct binding of microRNA-409 and ZNF366. RESULTS: The grip strength in both groups was temporarily decreased after surgery, while the grip strength in SCI group was always remarkably lower than that of the sham operation group since the first week after the surgery, suggesting the successful construction of mouse SCI model. MicroRNA-409 expression in the SCI group was gradually decreased from the postoperative 3rd day, which was remarkably lower than that of the sham group. Additionally, ZNF366 expression in the SCI group began to increase from the first day after the surgery, which was markedly higher than that of the sham group. After injection of exogenous microRNA-409, ZNF366 expression in the SCI group showed a remarkable decrease compared to that of the sham operation group. We also confirmed that ZNF366 was the target gene of microRNA-409 by bioinformatics analysis and luciferase activity assay. CONCLUSIONS: MicroRNA-409 is downregulated after spinal cord injury. Overexpression of microRNA-409 directly targets ZNF366 and promotes the recovery of spinal cord injury.

Study on the role of Hsa-miR-382-5p in epidural fibrosis.

OBJECTIVE: To investigate the role and potential mechanism of human serum albumin (hsa)-micro ribonucleic acid (miR)-382-5p in epidural fibrosis formation after laminectomy. MATERIALS AND METHODS: Cells were transfected with miR-382-5p mimic or miR-382-5p inhibitor. Then, 3-(4,5)-dimethylthiahiazol (-z-y1)-3,5-di-phenytetrazoliumromide (MTT) assay was employed to detect the effect of miR-382-5p on proliferation, and Real-time reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting were used to examine the expressions of miR-382-5p and fibrosis-related proteins after treatment with transforming growth factor beta (TGF-ß). Luciferase assay and immunofluorescent staining were done to confirm whether collagen I A1 is a target of miR-382-5p. RESULTS: MTT assay demonstrated that miR-382-5p had no significant effect on fibroblast proliferation. Expressions of miR-382-5p and fibrosis-related proteins were remarkably increased after TGF-ß treatment. Collagen I A1 was acknowledged as a target of miR-382-5p. MiR-382-5p mimic statistically enhanced the level of collagen I A1, and miR-382-5p enhanced the expressions of collagen I A1. CONCLUSIONS: Increased miR-382-5p promotes epidural fibrosis by increasing collagen I A1 expression, and miR-382-5p may be a potential novel molecular target for the treatment of epidural fibrosis.