p38MAPK及ERK信号通路激活在CD151促进内皮细胞迁移中的作用机制

Role of p38MAPK and ERK Signal Pathways in the CD151-promoted HUVECs Migration

目的研究p38MAPK信号通路及ERK信号通路激活在CD151促进人脐静脉内皮细胞(HUVECs)迁移中的机制。方法包装携带CD151、antiCD151和GFP的重组腺相关病毒,转染HUVECs。Western blot检测HUVECs中CD151、细胞外信号调节激酶(ERK)、p38丝裂原活化蛋白激酶(MAPK)蛋白的表达;利用改良的Boyden趋化小室进行细胞迁移检测;在细胞转染同时分别给予ERK抑制剂(PD98059,20μmol/L),或p38MAPK抑制剂(SB203580,20μmol/L),然后检测细胞迁移。结果 1 CD151组较空白对照组及GFP组明显促进细胞迁移的能力,而antiCD151组则显著抑制细胞的迁移,差异具有统计学意义(P<0.05)。2 CD151高表达促进ERK信号通路激活,而对p38MAPK信号通路无显著作用。3 ERK抑制剂(PD98059)显著抑制CD151转染后的促HUVECs迁移的作用(P<0.05),而p38MAPK抑制剂(SB203580)无明显作用。结论 CD151具有促进细胞迁移的作用,CD151通过激活ERK信号通路促进细胞迁移,而p38MAPK信号通路的激活则在CD151促进HUVECs迁移中无显著作用。

Objective To study the mechanism by which the activation of p38 MAPK and ERK signal pathways affects CD151-promoted migration of human umbilical vein endothelial cells（HUVECs）.Methods rAAV-CD151,rAAV-antiCD151 and rAAV-GFP were constructed and transfected into HUVECs.Protein expression levels of CD151,p38 MAPK and ERK were measured by Western blot.The migration of HUVECs was detected by using modified Boyden chamber assay.HUVECs were treated with ERK inhibitor（PD98059,20μmol/L）or p38 MAPK inhibitor（SB203580,20μmol/L）at the time of transfection and cell migration was determined.Results 1 Cell migration was significantly increased in CD151 group when compared with blank control and GFP groups.It was significantly inhibited in antiCD151 group.There was significant difference.2 Overexpression of CD151 activated ERK signal pathway but had no effect on p38 MAPK signal pathway.3 ERK inhibitor（PD98059）rather than p38 MAPK inhibitor（SB203580）could significantly suppress the CD151-induced HUVECs migration.Conclusion Activation of ERK signaling pathway,but not p38 MAPK,is involved in the CD151-induced HUVECs migration.