首页> 美国卫生研究院文献>Experimental and Therapeutic Medicine >Vascular endothelial growth factor participates in modulating the C6 glioma-induced migration of rat bone marrow-derived mesenchymal stem cells and upregulates their vascular cell adhesion molecule-1 expression
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Vascular endothelial growth factor participates in modulating the C6 glioma-induced migration of rat bone marrow-derived mesenchymal stem cells and upregulates their vascular cell adhesion molecule-1 expression

机译:血管内皮生长因子参与调节C6胶质瘤诱导的大鼠骨髓间充质干细胞迁移并上调其血管细胞粘附分子1表达

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摘要

Bone marrow-derived mesenchymal stem cells (BMSCs) have been shown to be able to migrate towards glioma, but the molecular mechanisms responsible for this migratory behavior still require further elucidation. This study aimed to test the role of vascular endothelial growth factor (VEGF) in the C6 glioma-induced migration of BMSCs, evaluate the effect of VEGF on the migratory capacity and vascular cell adhesion molecule-1 (VCAM-1) expression of BMSCs and explore the role of VCAM-1 in the VEGF-induced migration of BMSCs. The results showed that C6 glioma cells significantly increased the migration of BMSCs in vitro, which was partially blocked by a VEGF neutralizing antibody, and 20 ng/ml recombinant rat VEGF164 incubation enhanced the migration of BMSCs. Moreover, 12 h of 20 ng/ml VEGF164 incubation upregulated the VCAM-1 expression of BMSCs and the blocking of VCAM-1 reduced the VEGF164-induced migration of BMSCs. The data also revealed that , an inhibitor of phosphoinositide-3-kinase (PI3K), decreased the VEGF-induced migration and VCAM-1 expression of BMSCs. These findings indicate that VEGF participates in mediating the C6 glioma-induced migration of BMSCs by upregulating their VCAM-1 expression, and that PI3K is involved in the signal transduction of VEGF164-induced migration and VCAM-1 expression of BMSCs.
机译:骨髓间充质干细胞(BMSCs)已被证明能够向神经胶质瘤迁移,但是造成这种迁移行为的分子机制仍需要进一步阐明。这项研究旨在测试血管内皮生长因子(VEGF)在C6胶质瘤诱导的BMSC迁移中的作用,评估VEGF对BMSCs迁移能力和血管细胞粘附分子1(VCAM-1)表达的影响。探索VCAM-1在VEGF诱导的BMSC迁移中的作用。结果表明,C6胶质瘤细胞在体外显着增加了BMSCs的迁移,这部分被VEGF中和抗体所阻断,而20 ng / ml重组大鼠VEGF164的孵育增强了BMSCs的迁移。此外,在20 ng / ml VEGF164中孵育12小时可上调BMSCs的VCAM-1表达,而阻断VCAM-1可减少VEGF164诱导的BMSCs迁移。数据还显示,磷酸肌醇-3-激酶(PI3K)抑制剂可降低VEGF诱导的BMSCs迁移和VCAM-1表达。这些发现表明,VEGF通过上调它们的VCAM-1表达来参与介导C6神经胶质瘤诱导的BMSC的迁移,并且PI3K参与了VEGF164诱导的BMSC的迁移和VCAM-1表达的信号转导。

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