Abstract

B ackground: Periprosthetic osteolysis may lead to the failure of hip arthroplasty. The role of long non-coding RNA TUG1 in inducing periprosthetic osteolysis after hip arthroplasty remains unknown. M ethods: Clinical tissues were obtained from the patients undergoing hip arthroplasty. Mouse osteoblast cell line MC3T3-E1 was simulated by CoCrMo metal particles (CoPs). Real-time PCR was performed to determine the expression of TUG1 and BMP-7. Western blot was performed to determine the BMP-7 protein expression. Cell apoptosis was determined using flow cytometry. RNA pull-down was performed to determine the interaction between TUG1 and BMP-7. In vivo experiments were performed to verify the role of TUG1. R esults : Overexpressed TUG1 and down-regulated BMP-7 was observed in both clinical periprosthetic tissues and CoPs-stimulated osteoblasts. Knockdown of TUG1 significantly inhibited the apoptosis of CoPs-stimulated osteoblasts by targeting BMP-7. In vivo experiments verified that knockdown of TUG1 increased bone mineral density of the mouse osteolysis model. C onclusion: Knockdown of TUG1 inhibited the apoptosis of CoPs-stimulated osteoblasts by negatively regulating BMP-7, which might provide a new insight in treating periprosthetic osteolysis after hip arthroplasty. K eywords: periprosthetic osteolysis; TUG1; BMP-7; osteoblast apoptosis

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