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SDF Factor-1α Promotes the Migration, Proliferation, and Osteogenic Differentiation of Mouse Bone Marrow Mesenchymal Stem Cells Through the Wnt/β-Catenin Pathway
Stem Cells and Development ( IF 4 ) Pub Date : 2021-01-15 , DOI: 10.1089/scd.2020.0165
Zhiqiang Meng 1 , Gangning Feng 1 , Xueyu Hu 1 , Lvlin Yang 1 , Xiaochun Yang 1 , Qunhua Jin 1, 2
Affiliation  

Bone marrow mesenchymal stem cells (BMSCs) are thought to have great potential in the treatment of many diseases and may serve as a cell source for tissue engineering. These cells may be regulated by stromal cell-derived factor-1α (SDF-1α), which has been shown to promote the migration, proliferation, and osteogenic differentiation of BMSCs in inflammation-associated diseases. However, the specific mechanism underlying this process remains unclear. We herein transduced lentivirus carrying SDF-1α, empty vector, or siRNA-SDF-1α into mouse BMSCs and then performed transwell, CCK-8, cell cycle, alkaline phosphatase activity, and Alizarin Red staining experiments on the three groups of samples. Overexpression of SDF-1α promoted the migration, proliferation, and osteogenic differentiation of BMSCs, and SDF-1α upregulated the expression of Wnt pathway-related factors and downstream target genes as determined by western blot, real-time polymerase chain reaction, and immunofluorescence. The effect of low SDF-1α expression on BMSCs was significantly weakened. In addition, we transduced lentivirus carrying siRNA-Wnt3a into BMSCs and treated them with SDF-1 drugs. After inhibiting the Wnt pathway, SDF-1 significantly weakened the migration, proliferation, and osteogenic differentiation of BMSCs. From this, we concluded that high SDF-1 expression can promote the migration, proliferation, and osteogenic differentiation of BMSCs, at least in part by activating the Wnt pathway.

中文翻译:

SDF Factor-1α 通过 Wnt/β-Catenin 通路促进小鼠骨髓间充质干细胞的迁移、增殖和成骨分化

骨髓间充质干细胞 (BMSCs) 被认为在治疗许多疾病方面具有巨大潜力,并可作为组织工程的细胞来源。这些细胞可能受基质细胞衍生因子-1α (SDF-1α) 的调控,该因子已被证明可促进 BMSCs 在炎症相关疾病中的迁移、增殖和成骨分化。然而,这一过程的具体机制尚不清楚。我们在此将携带 SDF-1α、空载体或 siRNA-SDF-1α 的慢病毒转导到小鼠 BMSCs 中,然后对三组样品进行 transwell、CCK-8、细胞周期、碱性磷酸酶活性和茜素红染色实验。SDF-1α 的过表达促进了 BMSCs 的迁移、增殖和成骨分化,通过蛋白质印迹、实时聚合酶链反应和免疫荧光测定,SDF-1α 上调 Wnt 通路相关因子和下游靶基因的表达。SDF-1α低表达对BMSCs的影响显着减弱。此外,我们将携带 siRNA-Wnt3a 的慢病毒转导到 BMSCs 中,并用 SDF-1 药物处理它们。在抑制 Wnt 通路后,SDF-1 显着减弱了 BMSCs 的迁移、增殖和成骨分化。由此,我们得出结论,高 SDF-1 表达可以促进 BMSCs 的迁移、增殖和成骨分化,至少部分是通过激活 Wnt 途径。SDF-1α低表达对BMSCs的影响显着减弱。此外,我们将携带 siRNA-Wnt3a 的慢病毒转导到 BMSCs 中,并用 SDF-1 药物处理它们。在抑制 Wnt 通路后,SDF-1 显着减弱了 BMSCs 的迁移、增殖和成骨分化。由此,我们得出结论,高 SDF-1 表达可以促进 BMSCs 的迁移、增殖和成骨分化,至少部分是通过激活 Wnt 途径。SDF-1α低表达对BMSCs的影响显着减弱。此外,我们将携带 siRNA-Wnt3a 的慢病毒转导到 BMSCs 中,并用 SDF-1 药物处理它们。在抑制 Wnt 通路后,SDF-1 显着减弱了 BMSCs 的迁移、增殖和成骨分化。由此,我们得出结论,高 SDF-1 表达可以促进 BMSCs 的迁移、增殖和成骨分化,至少部分是通过激活 Wnt 途径。
更新日期:2021-01-15
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