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本室前期工作发现,单核细胞趋化蛋白-1(MCP-1)可诱导人内皮细胞(hVECs)凋亡.为进一步揭示MCP-1诱导凋亡分子机理,首先观察MCP-1对hVECs CC类趋化因子受体2(C-C motifchemokine receptor-2,CCR2)蛋白表达的影响.Western印迹结果显示,MCP-1以剂量依赖方式诱导CCR2在hVECs的表达.以脂质体为载体的CCR2反义寡核苷酸序列转染hVECs后,激光共聚焦显微镜及膜联蛋白(annexin)V-FITC/PI双染流式细胞术显示,CCR2反义寡核苷酸转染hVECs48h后可明显降低CCR2蛋白质的表达(P<0.05),抑制MCP-1诱导的hVECs凋亡(P<0.01).反义CCR2抑制凋亡结果与加入CCR2阻断剂RS102895后细胞凋亡测定结果一致.上述结果表明,MCP-1的主要受体CCR2介导了MCP-1诱导的hVECs凋亡.
Previous work showed that monocyte chemoattractant protein-1 (MCP-1) can induce apoptosis of human endothelial cells (hVECs) .To further reveal the molecular mechanism of MCP-1 induced apoptosis, we first observed the effect of MCP-1 on hVECs CC The expression of CCR2 was detected by Western blotting in a dose-dependent manner.The expression of CCR2 in hVECs was induced by lipopolysaccharide (CCR2) antisense After transfection of hVECs with oligonucleotide sequences, confocal laser scanning microscopy and Annexin V-FITC / PI double staining flow cytometry showed that CCR2 antisense oligonucleotides transfected hVECs 48h significantly reduced the expression of CCR2 protein (P <0.05), and inhibited the apoptosis of hVECs induced by MCP-1 (P <0.01) .The results of apoptosis inhibition of antisense CCR2 were the same as those of CCR2 inhibitor RS102895.The above results showed that MCP 1, a major receptor of CCR2, mediates apoptosis of hVECs induced by MCP-1.