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作 者:徐艳[1] 刘喜平[1] 李琴山[1] 尚惠锋[1] 钱民章[1]
机构地区:[1]贵州省遵义医学院生物化学教研室,贵州遵义563003
出 处:《中国生物化学与分子生物学报》2010年第4期356-361,共6页Chinese Journal of Biochemistry and Molecular Biology
基 金:国家自然科学基金项目(No.30760078)资助~~
摘 要: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.Our previous report demonstrated that monocyte chemotactic protein-1(MCP-1) inhibited the apoptosis of human vein endothelial cells(hVECs).To investigate the possible mechanisms,we evaluated the C-C motif chemokine receptor-2(CCR2) expression in hVECs.The Western blot results indicated that CCR2 was dose-dependently induced by MCP-1.When hVECs were transfected with CCR2 antisense oligodeoxynucleotide(ASODN) in lipofectamine reagent,the CCR2 expression was significantly reduced as indicated by laser scanning confocal microscopy and annexin V-FITC /PI double staining flow cytometry.The degree of apoptosis in hVECs was significantly inhibited(P 〈0.01) in 48 hours after CCR2-ASODN transfection.The CCR2 antagonist RS102895 showed the same effects as CCR2-ASODN on hVECs apoptosis.Our results suggested that CCR2 involved in MCP-1 induced apoptosis in hVECs.
关 键 词:单核细胞趋化因子1 CC类趋化因子受体2 人脐静脉内皮细胞 反义寡核苷酸 细胞凋亡
分 类 号:R329.2[医药卫生—人体解剖和组织胚胎学]
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