中文摘要：

目的探讨血管细胞黏附分子-1（VCAM-1）过表达对小鼠间充质干细胞（MSC）迁移能力的影响,并初步探讨其作用机制。方法将正常小鼠MSC（C3）、转染空载体的小鼠MSC（C3＋N）和基因修饰过表达VCAM-1的小鼠MSC（C3＋VCAM-1）分别接种在Transwell培养体系培养8和12 h,以胎牛血清为趋化物质诱导MSC迁移。甲紫（结晶紫）和DAPI染色法观察并计数各组细胞的迁移细胞数和迁移率。利用丝裂原活化蛋白激酶（MAPK）通路抑制剂〔SB203580,PD98059和Jun激酶（JNK）抑制剂Ⅱ〕阻断细胞活化的信号通路,观察各组MSC迁移能力的改变。结果 MSC在Transwell体系培养8和12 h,C3＋VCAM-1组细胞迁移数分别为7467±485和8795±255,迁移率分别为（14.9±1.0）%和（17.6±0.5）%,均显著高于C3组〔2731±562和4779±224;（5.5±1.1）%和（9.6±0.4）%〕和C3＋N组〔2539±321和5645±1080;（5.1±0.6）%和（11.3±1.1）%〕（P〈0.05,P〈0.01）。加入JNK抑制剂Ⅱ可抑制MSC的迁移能力,C3＋VCAM-1组迁移的细胞数为4843±167,迁移率为（9.7%±0.3）%,显著低于不加JNK抑制剂Ⅱ的C3＋VCAM-1组（P〈0.01）。MAPK通路抑制剂SB203580和PD98059对MSC的迁移能力无抑制作用。结论 VCAM-1过表达可能通过活化JNK/MAPK通路促进小鼠MSC的体外迁移作用。

英文摘要：

OBJECTIVE To investigate the effect of overexpression of vascular cell adhesion molecule-1（VCAM-1）on the migration in vitro of the murine mesenchymal stem cells（MSCs）and its possible mechanism.METHODS The migration ability of normal mouse MSC（C3）,empty vectortransfected MSC（C3＋N） and VCAM-1 transfected MSC（C3＋VCAM-1）was assessed by Transwell culture system in vitro after incubation for 8 and 12 h,respectively.The fetal bovine serum（FBS）was used as the chemotactic agent to induce MSC migration.The transmigrated cells were detected with methylosaniliam chloride（crystal violet）as well as DAPI staining.Furthermore,the specific chemical inhibitors of mitogen- activation protein kinase（MAPK） pathway（ SB203580,PD98059 and JNK inhibitorⅡ）were added to the Transwell system for 12 h and the alteration of the MSC migration ability was evaluated. RESULTS After incubation with FBS for 8 and 12 h,the absolute migrated cell number（7467±485 and 8795±255）and migration rate〔（14.9±1.0）% and（17.6±0.5）%〕 of MSC in C3＋VCAM-1 group were significantly increased compared with C3 group〔2731±562 and 4779±224,（5.5±1.1）% and（9.6±0.4）%〕 and C3＋N group〔2539±321 and 5645±1080,（5.1±0.6）% and（11.3±1.1）%〕（P〈0.05,P〈0.01）,but there was no significant difference between C3 and C3 ＋ N groups.Moreover,the MSC migration ability of C3＋VCAM-1 group was partially suppressed by addition of JNK inhibitorⅡ. The transmigrated cel number（4843±167）and migration rate〔（9.7±0.3）%〕were decreased compared with those of C3 ＋ VCAM- 1 group without JNK inhibitor Ⅱ（P〈0.01）. SB203580 and PD98059,as specific chemical inhibitors of MAPK pathway,had no effect on MSC migration. CONCLUSION VCAM- 1 can enhance mouse MSC migration in vitro and th4 e mechanism may be related to JNK/MAPK pathway activation.