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Downregulation of microRNA‐367 promotes osteoblasts growth and proliferation of mice during fracture by activating the PANX3‐mediated Wnt/β‐catenin pathway

A majority of people suffering from bone fractures fail to heal and develop a nonunion, which is a challenging orthopedic complication requiring complex and expensive treatment. Previous data showed the inhibition of some microRNAs (miRNAs or miRs) can enhance fracture healing. The objective of the present study is to explore effects of miR‐367 on the osteoblasts growth and proliferation of mouse during fracture via the Wnt/β‐catenin pathway by targeting PANX3. Primarily, the femur fracture model was successfully established in 66 (C57BL/6) 6‐week–old male mice. To verify whether miR‐367 target PANX3, we used the target prediction program and performed luciferase activity determination. Subsequently, to figure out the underlying regulatory roles of miR‐367 in fracture, osteoblasts were elucidated by treatment with miR‐367 mimic, miR‐367 inhibitor, or siRNA against PANX3 to determine the expression of miR‐367, siPANX3, β‐catenin, and Wnt5b as well as cell proliferation and apoptosis. The results demonstrated that PANX3 was verified as a target gene of miR‐367. MiR‐367 was found to highly expressed but PANX3, β‐catenin, and Wnt5b were observed poorly expressed in fracture mice. downregulated miR‐367 increased the mRNA and protein expression of PANX3, β‐catenin, and Wnt5b, increased cell growth, proliferation, and migration, while decreased cell apoptosis in osteoblasts. Altogether, our study demonstrates that the downregulation of miR‐367 may promote osteoblasts growth and proliferation in fracture through the activation of the PANX3‐dependent Wnt/β‐catenin pathway.