Enhanced osteogenic differentiation of human bone–derived mesenchymal stem cells in 3‐dimensional printed porous titanium scaffolds by static magnetic field through up‐regulating Smad4

间充质干细胞 体内 骨整合 体外 细胞生物学 脚手架 化学 生物医学工程 再生(生物学) 材料科学 生物 医学 生物化学 外科 植入 生物技术
作者
Yu He,Lingjia Yu,Jieying Liu,Yaqian Li,Yuanhao Wu,Zhenfei Huang,Di Wu,Hai Wang,Zhihong Wu,Guixing Qiu
出处
期刊:The FASEB Journal [Wiley]
卷期号:33 (5): 6069-6081 被引量:46
标识
DOI:10.1096/fj.201802195r
摘要

The reconstruction of large bone defects remains a significant challenge for orthopedists. Three-dimensional-printed (3DP) scaffold is considered a promising repair material. Static magnetic field (SMF) treatment is an effective and noninvasive therapeutic method to improve bone regeneration. However, the osteogenic effect of SMF on human bone-derived mesenchymal stem cells (hBMSCs) in 3DP scaffolds, as well as its potential mechanism, are unclear. In this study, the osteogenic effect of SMF on hBMSCs in a 3DP scaffold was investigated in vitro and in vivo. In addition, the potential mechanism for promoting osteogenesis was investigated by proteomic analysis. The results showed that SMF promoted osteogenic differentiation of hBMSCs in vitro. A total of 185 differential proteins were identified under SMF conditions by proteomic analysis. The osteogenic effect might be associated with bone morphogenetic protein-Smad1/5/8-signaling pathway and increased transport of phosphorylated Smad1/5/8 and phosphorylated Smad2/3 to the nucleus by up-regulating Smad4 under SMF conditions. The in vivo experiment showed that bone regeneration and osseointegration was enhanced by SMF in the rat model of bone defect. In conclusion, moderate SMF was a safe and effective method for enhancing osteogenesis in 3DP scaffolds in vitro and in vivo.-He, Y., Yu, L., Liu, J., Li, Y., Wu, Y., Huang, Z., Wu, D., Wang, H., Wu, Z., Qiu, G. Enhanced osteogenic differentiation of human bone-derived mesenchymal stem cells in 3-dimensional printed porous titanium scaffolds by static magnetic field through up-regulating Smad4.

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