A major challenge in bone tissue engineering is the lack of post-implantation vascular growth into biomaterials. In the skeletal system, blood vessel growth appears to be coupled to osteogenesis-suggesting the existence of molecular crosstalk between endothelial cells (ECs) and osteoblastic cells. The present study (performed in two murine ectopic models) was designed to determine whether co-transplantation of human Wharton's jelly mesenchymal stem cell-derived osteoblasts (WJMSC-OBs) and human differentiated ECs enhances bone regeneration and stimulates angiogenesis, relative to the seeding of WJMSC-OBs alone. Human WJMSC-OBs and human ECs were loaded into a silicate-substituted calcium phosphate (SiCaP) scaffold and then ectopically implanted at subcutaneous or intramuscular sites in nude mice. At both subcutaneous and intramuscular implantation sites, we observed ectopic bone formation and osteoids composed of host cells when WJMSC-OBs were seeded into the scaffold. However, the addition of ECs was associated with a lower level of osteogenesis, and we did not observe stimulation of blood vessel ingrowth. in vitro studies demonstrated that WJMSC-OBs lost their ability to secrete vascular endothelial growth factor and stromal cell-derived factor 1-including when ECs were present. In these two murine ectopic models, our cell-matrix environment combination did not seem to be optimal for inducing vascularized bone reconstruction.

中文翻译：

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沃顿氏胶质间充质干细胞衍生的成骨细胞与分化的内皮细胞的共同移植不会刺激裸鼠模型中的血管和类骨质形成。

骨组织工程学中的主要挑战是植入后的血管缺乏向生物材料的生长。在骨骼系统中，血管的生长似乎与成骨有关，这暗示着内皮细胞（EC）和成骨细胞之间存在分子串扰。本研究（在两个鼠异位模型中进行）旨在确定人沃顿氏胶质间充质干细胞来源的成骨细胞（WJMSC-OBs）和人分化的内皮细胞是否共同移植，相对于仅WJMSC-OB。将人类WJMSC-OB和人类EC加载到硅酸盐取代的磷酸钙（SiCaP）支架中，然后异位植入裸鼠的皮下或肌肉内部位。在WJMSC-OBs植入支架时，我们在皮下和肌内植入部位均观察到异位骨形成和类固醇，后者由宿主细胞组成。但是，ECs的添加与成骨水平降低有关，我们没有观察到血管向内生长的刺激。体外研究表明，当存在EC时，WJMSC-OB失去了分泌血管内皮生长因子和基质细胞衍生因子1的能力。在这两种鼠异位模型中，我们的细胞-基质环境组合似乎并不是诱导血管化骨重建的最佳方法。而且我们没有观察到血管向内生长的刺激。体外研究表明，当存在EC时，WJMSC-OB失去了分泌血管内皮生长因子和基质细胞衍生因子1的能力。在这两种鼠异位模型中，我们的细胞-基质环境组合似乎并不是诱导血管化骨重建的最佳方法。而且我们没有观察到血管向内生长的刺激。体外研究表明，当存在EC时，WJMSC-OB失去了分泌血管内皮生长因子和基质细胞衍生因子1的能力。在这两种鼠异位模型中，我们的细胞-基质环境组合似乎并不是诱导血管化骨重建的最佳方法。