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BACKGROUND: This study is based on the evidence that bone morphogenetic protein 2 plays an important role in osteogenesis and bone repair, and Schnurri3 can regulate the transforming growth factor-β signal transduction. OBJECTIVE: To investigate the effect of inhibiting Schnurri3 on bone morphogenetic protein 2-induced osteogenic differentiation of C3H10T1/2 cells. METHODS: Mouse mesenchymal stem cell line C3H10T1/2 cells were used as research materials. Four groups were set in this study: adenovirus-green fluorescent protein, adenovirus-bone morphogenetic protein 2, adenovirus-Simshn3 and adenovirus-bone morphogenetic protein 2+adenovirus-Simshn3. The expression of bone morphogenetic protein 2 was enhanced and the expression of Schnurri3 was inhibited. Alkaline phosphatase staining was used to detect the expression of alkaline phosphatase. The mRNA transcriptional levels of bone morphogenetic protein 2, Schnurri3, osteogenic and angiogenic markers were determined by RT-qPCR. Immunohistochemical staining was used to detect the expression of type I collagen, vascular endothelial growth factor and endothelial mucin. Alizarin red staining and semiquantitative analysis were used to detect calcium salt deposition levels. Subcutaneous stem cell implantation in nude mice was used to measure ectopic bone. RESULTS AND CONCLUSION: (1) Recombinant adenovirus-bone morphogenetic protein 2 could induce osteogenic differentiation of C3H10T1/2 cells. Compared with the adenovirus-bone morphogenetic protein 2 group, mRNA transcription levels of osteogenic markers alkaline phosphatase, type I collagen, osteoblast-specific transcription factor, osteocalcin, Runt related transcription factor 2 and angiogenic markers neurite guidance factor, vascular endothelial growth factor, von Willebrand factor, angiopoietin and endothelial mucin were significantly increased in the adenovirus-bone morphogenetic protein 2+adenovirus-Simshn3 group (P < 0.001). Simultaneously, it significantly enhanced the expression of type I collagen, vascular endothelial growth factor and endothelial mucin at the protein level (P < 0.05), and the calcium salt deposition level (P < 0.05). (2) The application of bone morphogenetic protein 2 and Schnurri3 alone could act on C3H10T1/2 cells to form ectopic bone blocks subcutaneously in nude mice. Bone morphogenetic protein 2 combined with Schnurri3 could form more significant ectopic bone blocks. (3) The results showed that inhibition of Schnurri3 significantly enhanced the osteogenic differentiation of C3H10T1/2 cells induced by bone morphogenetic protein 2, and enhanced the expression of angiogenesis factors mRNA and protein to regulate angiogenesis. [ABSTRACT FROM AUTHOR]

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