Autologous oxygen release nano bionic scaffold composite miR-106a induced BMSCs enhances osteoblast conversion and promotes bone repair through regulating BMP-2.

Abstract

Suitable seed cells and selection of bioactive scaffold materials are the main research contents of bone tissue engineering. It was showed that autologous oxygen release nano bionic scaffold could promote the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). The role of microRNA-106a (miR-106a) in regulating BMSCs differentiation has not been reported. We intend to investigate the role of autologous oxygen release nano bionic scaffold composite miR-106a in inducing BMSCs constructing tissue engineering bone. Rat BMSCs were isolated and transfected by using miR-106a scramble or miR-106a inhibitor. Healthy male Sprague-Dawly (SD) rats were randomly divided into three groups, including bone fracture group established as rat tibial fracture model, negative control group implanted by autologous oxygen release nano bionic scaffold composite miR-106a scramble BMSCs, and miR-106a inhibitor group implanted by autologous oxygen release nano bionic scaffold composite miR-106a inhibitor BMSCs. Callus growth was observed. Alkaline phosphatase (ALP) activity was detected. Bone morphogenetic protein 2 (BMP-2) expression was tested by Real-time PCR (RT-PCR) and Western blot assay. Collagen II production was determined by RT-PCR. Autologous oxygen release nano bionic scaffold composite BMSCs significantly increased local bone mineral density, promoted callus healing, facilitated ALP secretion, elevated collagen II expression, and up-regulated BMP-2 mRNA and protein levels compared with fracture group (p<0.05). Autologous oxygen release nano bionic scaffold composite miR-106a induced BMSCs exhibited more significant effect on bone repair (p<0.05). Autologous oxygen release nano bionic scaffold composite miR-106a induced BMSCs enhanced osteoblast conversion and promoted bone repair through regulating BMP-2.