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作 者:钟久昌[1,2] 余细勇[2] 郭俊明[1] 林秋雄[2] 龚朝辉[1] 刘琼[1]
机构地区:[1]宁波大学医学院分子高血压病研究室,生物化学与分子生物学研究所,浙江宁波315211 [2]广东省人民医院医学研究中心,广东广州510080
出 处:《中国病理生理杂志》2008年第10期1922-1926,共5页Chinese Journal of Pathophysiology
基 金:国家自然科学基金资助项目(No.30700328);广东省自然科学基金资助项目(No.7300041);宁波市自然科学基金资助项目(No.2008A610077)
摘 要:目的:探讨重组血管紧张素转换酶2(ACE2)基因转染对体外培养的人血管内皮细胞中由血管紧张素(Ang)II诱导的巨噬细胞移动抑制因子(MIF)表达的影响。方法:克隆和构建含人ACE2基因全长的重组质粒(pACE2),并将之转染入人血管内皮细胞中。分别采用实时定量PCR和Western印迹技术检测转染细胞中的MIFmRNA与蛋白表达情况。结果:AngⅡ(100nmol/L)和AngIV(100nmol/L)刺激后均可诱导人血管内皮细胞中MIFmRNA及蛋白表达增加(P<0.01)。pACE2基因转染可明显抑制内皮细胞中由AngII和AngIV诱导的MIFmRNA和蛋白表达(P<0.05)。结论:ACE2基因过表达可明显抑制人内皮细胞中炎症介质MIF的表达,提示ACE2基因具有一定的抗炎症效应。通过调节ACE2基因的活性和表达,很可能为炎症相关疾病如动脉粥样硬化治疗提供新的策略。AIM: To implore the effects of recombinant angiotensin - converting enzyme 2 (ACE2) gene transfection on the expression of macrophage migration inhibitory factor (MIF) induced by angiotensin (Ang) Ⅱ in cultured human endothelial cells. METHODS : A recombinant plasmid encompassing human ACE2 gene (pACE2) was constructed and transfected into human endothelial cells. Endothelial cells were stimulated with Ang Ⅱ or Ang Ⅳ in the presence and absence of pACE2 gene transfer. The mRNA and protein levels of MIF in endothelial cells were determined by real - time PCR and Western blotting, respectively. RESULTS : The mRNA and protein expressions of MIF were strikingly enhanced after exposures of endothelial cells to 100 nmol/L Ang Ⅱ and 100 nmol/L Ang Ⅳ(P 〈0. 01, respectively). However, significant downregnlations of MIF mRNA and protein expression were observed in endothelial cells pretreated with pACE2 gene transfer (P 〈 0. 05, respectively). CONCLUSION : ACE2 gene overexpression contributes to diminishments of inflammatian mediator MIF expression in endothelial cells, suggesting that ACE2 gene has anti - inflammatory properties to some extent and may provide novel therapeutic strategies for the inflammation- related diseases such as atherosclerosis.
关 键 词:血管紧张素转换酶2 巨噬细胞游走抑制因子 血管紧张素Ⅱ 炎症
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