趋化因子Fractalkine在血管紧张素II诱导内皮细胞ICAM-1表达中的作用

目的 研究Fractalkine（FKN）在血管紧张素II（Ang II）诱导内皮细胞表达细胞间黏附分子-1（ICAM-1）中的作用.方法 取人脐静脉内皮细胞（HUVECs）培养,分别给予低、高浓度（10-7 mol/L,10-6 mol/L）Ang II干预12、24、48 h,采用MTT检测内皮细胞活性,Western blot检测ICAM-1和FKN蛋白表达;小RNA转染内皮细胞后,用高浓度Ang II培养24 h并检测各组细胞FKN mRNA表达及ICAM-1和FKN蛋白表达.结果 Ang II可降低HUVECs活性并促进ICAM-1及FKN蛋白表达,高浓度AngII对内皮细胞活性影响较大;FKN siRNA转染可显著抑制FKN mRNA表达,且在高浓度Ang II作用24 h后,被转染细胞的FKN mRNA表达量仍显著低于阴性对照＋Ang II组（P＜0.05）,且ICAM-1及FKN蛋白表达显著减少.结论 Ang II可降低内皮细胞活性并促进内皮细胞ICAM-1和FKN蛋白表达,趋化因子FKN介导了Ang II诱导的内皮细胞ICAM-1蛋白表达过程.

Role of fractalkine in intercellular adhesion molecular-1 expression of human umbilical vein cells induced by angiotensin II

Objective To investigate the role of fractalkine （FKN） in intercellular adhesion molecule-1 （ ICAM-1 ） expression of human umbilical vein cells induced by angiotensin II. Methods Human umbilical vein endothelial cells （HUVECs） were incuba- ted with angiotensin II in two concentrations （ 10-7 mol/L, 10-6 tool/L） for 12 hours, 24 hours, and 48 hours. The change of cell via- bility was detected through methyl thiazole tetrazolium （MTr）. Cells were transfected with small interfering RNA （siRNA） of FKN by lipofectamine 2000. FKN mRNA expression was detected by real time quantitative polymerase chain reaction （RT-PCR）. The protein expressions of ICAM-1 and FKN were measured by Western blotting. Results Cell viability was decreased after angiotensin II treat- ment, angiotensin II of 10-6 mol/L was more effective in attenuating cell viability, the protein expressions of FKN and ICAM-1 were enhanced by angiotensin II after incubation for 12, 24, and 48 hours. FKN siRNA transfection inhibited FKN mRNA expression. Though the transfected HUVECs were incubated with angiotensin II （10-6 mol/L） for 24 hours, the protein expressions of FKN and ICAM-1 were largely decreased. Conclusions Angiotensin II can affect HUVECs viability and enhance the protein expressions of FKN and ICAM-1. Silence FKN gene can decrease the protein expressions of FKN and ICAM-1 in angiotensin II-induced HUVECs, FKN protein may participate in the angiotensin II-ICAM-1 pathway.