Vascularization is a prerequisite for bone formation. Endothelial progenitor cells (EPCs) stimulate bone formation by creating a vascular network. Moreover, EPCs secrete various bioactive molecules that may regulate bone formation. The aim of this research was to shed light on the pathways of EPCs in bone formation. In a subcutaneous nude mouse ectopic bone model, the transplantation of human EPCs onto β-TCP scaffold increased angiogenesis (p < 0.001) and mineralization (p < 0.01), compared to human neonatal dermal fibroblasts (HNDF group) and a-cellular scaffold transplantation (β-TCP group). Human EPCs were lining blood vessels lumen; however, the majority of the vessels originated from endogenous mouse endothelial cells at a higher level in the EPC group (p < 01). Ectopic mineralization was mostly found in the EPCs group, and can be attributed to the recruitment of endogenous mesenchymal cells ten days after transplantation (p < 0.0001). Stromal derived factor-1 gene was expressed at high levels in EPCs and controlled the migration of mesenchymal and endothelial cells towards EPC conditioned medium in vitro. Blocking SDF-1 receptors on both cells abolished cell migration. In conclusion, EPCs contribute to osteogenesis mainly by the secretion of SDF-1, that stimulates homing of endothelial and mesenchymal cells. This data may be used to accelerate bone formation in the future.

中文翻译：

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内皮细胞的旁分泌作用通过CXCR4 / SDF-1途径在骨形成中的作用。

血管化是骨形成的前提。内皮祖细胞（EPC）通过创建血管网络来刺激骨骼形成。此外，EPC分泌各种可能调节骨骼形成的生物活性分子。这项研究的目的是阐明EPC在骨骼形成中的途径。在皮下裸鼠异位骨模型中，与人新生儿真皮成纤维细胞（HNDF组）和a细胞支架移植相比，将人EPCs移植到β-TCP支架上可增加血管生成（p <0.001）和矿化（p <0.01）。 （β-TCP组）。人类EPC正在衬砌血管腔。然而，在EPC组中，大多数血管来自较高水平的内源性小鼠内皮细胞（p<01）。异位矿化多见于EPCs组，可归因于移植后10天内源性间充质细胞的募集（p <0.0001）。基质基质衍生因子-1基因在EPC中高水平表达，并在体外控制间充质和内皮细胞向EPC条件培养基的迁移。阻断两个细胞上的SDF-1受体消除了细胞迁移。总之，EPC主要通过SDF-1的分泌促进成骨，SDF-1的分泌刺激内皮细胞和间充质细胞的归巢。将来，该数据可用于加速骨骼形成。