Expression of miR-182 in patients with fracture of tibial plateau and its regulative effects on the fracture healing

Z.-W. Yan, P. Du, W. Zhang, W.-C. Sun, L. Jia, M. Jiang, Y. Liu, H.-L. Guo

Department of Rehabilitation Medicine, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, Heilongjiang, P.R. China. y0107zw@126.com

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• Orthopedics

OBJECTIVE: To investigate the expression of miR-182 in patients with fracture of tibial plateau (FTP) and its effects on osteoblasts and fracture healing.

PATIENTS AND METHODS: The patients with fracture of tibial plateau treated in our hospital and healthy subjects who received physical examination from January 2017 to January 2018 were collected. The expression of miR-182 in the serum was detected. The osteoblasts from SD rats were cultured and transfected with miR-182, anti-miR-182, miR-NC or anti-miR-NC using transfection reagent LipofectamineTM 2000. The proliferation, alkaline phosphatase (ALP) activity, calcification and osteogenic gene expression of osteoblasts were detected. The rat models with fracture of tibial plateau were divided into control group, fracture group, fracture+miR-182 group, and fracture+anti-miR-182 group. The levels of vascular endothelial growth factor (VEGF), epidermal growth factor (EGF) and transforming growth factor β (TGFβ) in serum were detected by enzyme-linked immunosorbent assay (ELISA).

RESULTS: Compared with the controls, the expression of miR-182 in serum was significantly elevated in patients with fracture of tibial plateau. Overexpression of miR-182 inhibited the proliferation of osteoblasts, while the knockdown of miR-182 increased the proliferation. MiR-182 could decrease the ALP activity of osteoblasts, while anti-miR-182 increased the ALP activity. Osteoblast calcification ability was significantly decreased by overexpression of miR-182. Knockdown of miR-182 increased the calcification ability of osteoblasts and the expression of osteogenic genes. MiR-182 could inhibit the expression of osteogenic genes. The levels of VEGF, EGF and TGFβ in the fracture group were higher than those in the control group, while the levels in the fracture+miR-182 group were higher than those in the fracture group. The levels of VEGF, EGF and TGFβ in the anti-miR-182 group were lower than those in the fracture group.

CONCLUSIONS: MiR-182 is elevated in patients with fracture of tibial plateau, which can inhibit the proliferation and differentiation of osteoblasts and affect the fracture healing. The knockdown of miR-182 might be a new method for treating fracture healing.

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