内脂素促进巨噬细胞向致血栓表型转化  

Visfatin Promoted Macrophages Conversion to a Thrombogenic Phenotype Independent of Insulin Receptor Signalling

作　　者：张高峰[1] 许澎[1] 乔祺[1] 

机构地区：[1]复旦大学附属上海市第五人民医院心内科,上海市200240

出　　处：《中国分子心脏病学杂志》2010年第6期356-359,共4页Molecular Cardiology of China

摘　　要：目的研究内脂素对巨噬细胞中组织因子(TF)和纤溶酶原激活物抑制剂-1(PAI-1)表达的影响及可能的机制。方法体外培养的THP-1细胞中加入不同浓度的内脂素(包括空白对照,50ng/ml,100ng/ml三个浓度组),每组分别孵育6小时,12小时和24小时各3个时间点。同时设立2-羟基萘甲基磷酸三乙酸甲基酯(HNMPA;100umol/L)组。将各组细胞进行realtime PCR和Western blot检测,比较各组TF和PAI-1表达的情况。结果内脂素增加巨噬细胞中TF和PAI-1的mRNA转录和蛋白质表达水平,HNMPA不影响内脂素的这些效应。结论内脂素促进巨噬细胞向促血栓表型转化,机制与胰岛素受体相关的途径无关。Objective To investigate effects of visfatin on expression of TF and PAI-1 in macrophages and related mechanism.Methods We treated THP-1-derived macrophages with visfatin ranged from 0 to100ng/ml for 6 to 24 hours,and tested mRNA expression and protein production of TF and PAI-1 by realtime quantified-PCR and Western blot analysis respectively.By administering HNMPA-an insulin receptor antagonist,we intended to determine whether visfatin influence TF and PAI-1 expressions through insulin receptor signalling.Results We showed that visfatin enhanced mRNA expression and protein production of TF and PAI-1 in macrophages(p<0.05),and HNMPA did not inhibit these effects.Conclusion We demonstrated that visfatin could promote macrophages conversion to a thrombogenic phenotype independent of insulin receptor signalling,which might be one of mechanisms underlying plaque vulnerability in atherosclerosis.

关 键 词：内脂素 巨噬细胞 血栓形成 动脉粥样硬化 

分 类 号：R363[医药卫生—病理学]