首页> 外文期刊>Journal of bone and mineral metabolism >SDF-1 mediates mesenchymal stem cell recruitment and migration via the SDF-1/CXCR4 axis in bone defect
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SDF-1 mediates mesenchymal stem cell recruitment and migration via the SDF-1/CXCR4 axis in bone defect

机译:SDF-1通过SDF-1 / CXCR4轴介导间充质干细胞募集和迁移在骨缺损中

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Introduction Recent studies have indicated the potential of stem cell therapy in combination with cytokines to restore the bone repair via migration and homing of stem cells to the defected area. The present study aimed to investigate the mobilization and recruitment of mesenchymal stem cells (MSCs) in response to SDF-1. Materials and Methods Herein, the knockout rat model of the bone defect (BD) was treated with the induced membrane technique. Then, wild type Wistar rats and SDF-1-knockout rats were selected for the establishment of BD-induced membrane (BD-IM) models and bone-graft (BG) models. The number of MSCs was evaluated by flow cytometry, along with the expression pattern of the SDF-1/CXCR4 axis as well as osteogenic factors was identified by RT-qPCR and Western blot analyses. Finally, the MSC migration ability was assessed by the Transwell assay. Results Our data illustrated that in the induced membrane tissues, the number of MSCs among the BD-IM modeled rats was increased, whereas, a lower number was documented among BG modeled rats. Besides, we found that lentivirus-mediated over-expression of SDF-1 in BG modeled rats could activate the SDF-1/CXCR4 axis, mobilize MSCs into the defect area, and up-regulate the osteogenic proteins. Conclusions Collectively, our study speculated that up-regulation of SDF-1 promotes the mobilization and migration of MSCs through the activation of the SDF-1/CXCR4 signal pathway.
机译:导言最近的研究表明,干细胞疗法与细胞因子相结合,通过干细胞向缺损区迁移和归巢来恢复骨修复的潜力。本研究旨在研究SDF-1对间充质干细胞(MSCs)的动员和募集作用。材料和方法:采用诱导膜技术处理基因敲除大鼠骨缺损(BD)模型。然后,选择野生型Wistar大鼠和SDF-1基因敲除大鼠建立BD诱导膜(BD-IM)模型和骨移植(BG)模型。流式细胞术检测骨髓间充质干细胞的数量,RT-qPCR和Western blot分析鉴定SDF-1/CXCR4轴的表达模式以及成骨因子。最后,通过Transwell分析评估MSC的迁移能力。结果我们的数据表明,在诱导的膜组织中,BD-IM模型大鼠的MSC数量增加,而BG模型大鼠的MSC数量减少。此外,我们发现慢病毒介导的SDF-1在BG模型大鼠中的过度表达可以激活SDF-1/CXCR4轴,动员MSC进入缺损区,并上调成骨蛋白。结论总体而言,我们的研究推测SDF-1的上调通过激活SDF-1/CXCR4信号通路促进MSC的动员和迁移。

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