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Expression of Renin–Angiotensin System on Dendritic Cells of Patients with Coronary Artery Disease

机译:肾素-血管紧张素系统在冠状动脉疾病患者树突状细胞中的表达

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Dendirtic cells (DCs) and renin–angiotensin system (RAS) have both been reported to contribute to the pathogenesis of atherosclerosis. Recently researches find the RAS expression on DCs and its effect on DCs’ differentiation and proinflammatory function. The pattern of RAS expression on DCs derived from normal monocytes vs that on DCs derived from cornoary artery diease was investigated. In 82 coronary artery disease (CAD) patients and healthy controls (CTL), expressions of angiotensin I-converting enzyme (ACE), angiotensin AT1 receptor and DC-specific ICAM-3-grabbing nonintegrin (DC-SIGN) on DCs were measured by western-blot: CAD patients had an increased expression of ACE, AT1 receptor and DC-SIGN compared to controls especially in acute myocardial infarction (AMI). Cardiovascular risk factors of cardiovascular disease and circulating anigotensin II (Ang II) were assessed and found increased in AMI compared with CTL. The DC-SIGN and high-sensitivity C-reactive protein (hsCRP) also had significant correlations with RAS expression on DCs. Our research demonstrated the RAS expressions on DCs and their increase in CAD especially AMI. The RAS activation on DCs may cause a series of changes such as enhancing recruitment of DCs, activating the T cells and increasing their proinflammtory functions. The recruitment and T cells contact ability of DCs increases through DC-SIGN may be one of pathogenesis of atherosclerosis and this function may promoted by tissue RAS. CRP may also have some effect to the local RAS exprssion on DCs.
机译:据报道树突状细胞(DCs)和肾素-血管紧张素系统(RAS)都有助于动脉粥样硬化的发病。最近的研究发现RAS在DC上的表达及其对DC分化和促炎功能的影响。研究了来自正常单核细胞的DC与来自角膜动脉疾病的DC的RAS表达模式。在82例冠状动脉疾病(CAD)患者和健康对照(CTL)患者中,通过DC测定了血管紧张素转换酶(ACE),血管紧张素AT1受体和DC特异性ICAM-3-抓整合素(DC-SIGN)的表达。 Western blot:与对照组相比,CAD患者的ACE,AT1受体和DC-SIGN的表达增加,尤其是在急性心肌梗塞(AMI)中。评估了心血管疾病和循环血管紧张素II(Ang II)的心血管危险因素,发现与CTL相比,AMI的患病风险增加。 DC-SIGN和高敏C反应蛋白(hsCRP)也与DC上的RAS表达有显着相关性。我们的研究证明了RAS在DC上的表达及其在CAD(尤其是AMI)中的表达。 DC上的RAS激活可能引起一系列变化,例如增强DC的募集,激活T细胞并增加其促炎功能。通过DC-SIGN增加DC的募集和T细胞接触能力可能是动脉粥样硬化的发病机理之一,并且该功能可能由组织RAS促进。 CRP也可能对DC上的本地RAS表示有一定影响。

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