Glioma Cells Promote the Expression of Vascular Cell Adhesion Molecule-1 on Bone Marrow-Derived Mesenchymal Stem Cells: a Possible Mechanism for Their Tropism Toward Gliomas
Glioma Cells Promote the Expression of Vascular Cell Adhesion Molecule-1 on Bone Marrow-Derived Mesenchymal Stem Cells: a Possible Mechanism for Their Tropism Toward Gliomas
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胶质瘤细胞促进骨髓间充质干细胞上血管细胞粘附分子1的表达：其向胶质瘤趋向的可能机制
DOI：
10.1007/s12031-012-9784-7
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发表时间：
2012-09-01
影响因子：
3.1
通讯作者：
Liu, Yun-Hui
中科院分区：
文献类型：
--
作者：
Hu, Yi;Cheng, Peng;Liu, Yun-Hui
骨髓间充质干细胞（BMSCs）对胶质瘤的趋化性已被体外和体内实验所证实。本研究旨在探讨血管细胞粘附分子-1（VCAM-1）在BMSCs向胶质瘤迁移中的作用及胶质瘤细胞对BMSCs VCAM-1表达的影响。根据其对塑料的粘附性分离BMSCs。采用体外迁移实验分析BMSCs对C6和U87胶质瘤的趋化性及VCAM-1在BMSCs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BMSCs与C6和U87胶质瘤细胞条件培养液（CM）共同孵育后VCAM-1的表达。数据显示，C6和U87胶质瘤细胞促进BMSC的迁移，这可以被VCAM-1中和抗体阻断。此外，VCAM-1的BMSCs的表达通过其CM的孵育而升高。磷脂酰肌醇-3-激酶（PI 3 K）抑制剂LY 294002可显著抑制胶质瘤诱导的BMSCs表面VCAM-1表达上调。提示胶质瘤诱导BMSCs VCAM-1表达的改变可能在BMSCs向胶质瘤的趋化性中起重要作用，PI 3 K参与了这一过程的信号转导。
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.