Li Fei, Guo Wen-yi, Li Wei-jie, Zhang Dian-xin, Lv An-lin, Luan Rong-hua, Liu Bing, Wang Hai-chang
Department of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Biochem Biophys Res Commun. 2009 Aug 14;386(1):247-51. doi: 10.1016/j.bbrc.2009.06.025. Epub 2009 Jun 11.
Cyclic stretch (CS) mediates different cellular functions in vascular smooth muscle cells and involves in neointimal hyperplasia and subsequent atherosclerosis of vein grafts. Here, we investigated whether CS can modulate stromal cell-derived factor-1alpha (SDF-1alpha)/CXCR4 axis in human saphenous vein smooth muscle cells. We found CS induced the upregulation of SDF-1alpha and CXCR4 in human saphenous vein smooth muscle cells in vitro, which was dependent on PI3K/Akt/mTOR pathway. Furthermore, CS augmented human saphenous vein smooth muscle migration and focal adhesion kinase (FAK) activation by PI3K/Akt/mTOR pathway. Interestingly, the upregulation of SDF-1alpha/CXCR4 axis was instrumental in CS-induced saphenous vein smooth muscle cell migration and FAK activation, as showed by AMD3100, an inhibitor of SDF-1alpha/CXCR4 axis, partially but significantly blocked the CS-induced cellular effects. Thus, those data suggested SDF-1alpha/CXCR4 axis involves in CS-mediated cellular functions in human saphenous vein smooth muscle cells.
周期性拉伸（CS）介导血管平滑肌细胞的不同细胞功能，并参与静脉移植物的新生内膜增生及随后的动脉粥样硬化。在此，我们研究了CS是否能调节人隐静脉平滑肌细胞中的基质细胞衍生因子-1α（SDF-1α）/CXCR4轴。我们发现CS在体外诱导人隐静脉平滑肌细胞中SDF-1α和CXCR4的上调，这依赖于PI3K/Akt/mTOR途径。此外，CS通过PI3K/Akt/mTOR途径增强人隐静脉平滑肌迁移和粘着斑激酶（FAK）激活。有趣的是，SDF-1α/CXCR4轴的上调有助于CS诱导的隐静脉平滑肌细胞迁移和FAK激活，如SDF-1α/CXCR4轴抑制剂AMD3100部分但显著阻断CS诱导的细胞效应所示。因此，这些数据表明SDF-1α/CXCR4轴参与CS介导的人隐静脉平滑肌细胞的细胞功能。
