Department of Neurosurgery, Shengjing Hospital, China Medical University, No.36, Sanhao Street, Heping District, Shenyang, Liaoning Province, 110004, People's Republic of China.
J Mol Neurosci. 2012 Sep;48(1):127-35. doi: 10.1007/s12031-012-9784-7. Epub 2012 May 6.
The tropism of bone marrow-derived mesenchymal stem cells (BMSCs) toward gliomas has been shown by in vitro and in vivo assays. This study was carried out to evaluate the role of vascular cell adhesion molecule-1 (VCAM-1) in the migration of BMSCs towards glioma and the effect of glioma cells on the VCAM-1 expression of BMSCs. BMSCs were isolated according to their adherence to plastic. The tropism of BMSCs toward C6 and U87 glioma and the role of VCAM-1 in this migration were analyzed by in vitro migration assay, separately. Reverse transcription-polymerase chain reaction, immunofluorescence, and Western blot were employed to assess VCAM-1 expression of BMSCs when they were incubated by the conditioned mediums (CM) of C6 or U87 glioma cells. Data revealed that C6 and U87 glioma cells promote the migration of BMSCs, which could be blocked by a VCAM-1-neutralizing antibody. Moreover, VCAM-1 expression of BMSCs was elevated by the incubation of their CM. The results also demonstrated that LY294002, an inhibitor of phosphoinositide-3-kinase (PI3K), significantly inhibited the glioma-induced upregulation of VCAM-1 on BMSCs. These findings suggested that glioma-induced change in VCAM-1 expression of BMSCs may play an important role in their tropism towards glioma, and PI3K is associated with the signal transduction of this process.
骨髓间充质干细胞（BMSCs）向神经胶质瘤的趋化性已在体外和体内实验中得到证实。本研究旨在评估血管细胞黏附分子-1（VCAM-1）在 BMSCs 向神经胶质瘤迁移中的作用，以及神经胶质瘤细胞对 BMSCs 中 VCAM-1 表达的影响。根据细胞对塑料的黏附性分离 BMSCs。通过体外迁移实验分别分析 BMSCs 向 C6 和 U87 神经胶质瘤的趋化性以及 VCAM-1 在这种迁移中的作用。采用逆转录-聚合酶链反应、免疫荧光和 Western blot 检测 C6 或 U87 神经胶质瘤细胞条件培养基孵育后 BMSCs 中 VCAM-1 的表达。结果表明，C6 和 U87 神经胶质瘤细胞促进了 BMSCs 的迁移，而 VCAM-1 中和抗体可阻断这种迁移。此外，BMSCs 的 CM 孵育可上调 VCAM-1 的表达。研究结果还表明，PI3K 抑制剂 LY294002 可显著抑制神经胶质瘤诱导的 BMSCs 中 VCAM-1 的上调。这些发现表明，神经胶质瘤诱导的 BMSCs 中 VCAM-1 表达的变化可能在其向神经胶质瘤的趋化性中发挥重要作用，而 PI3K 与该过程的信号转导有关。
