Interleukin-1 beta in coronary arteries of patients with ischemic heart disease
Interleukin-1 beta in coronary arteries of patients with ischemic heart disease
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DOI：
10.1161/01.atv.16.8.1000
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发表时间：
1996-08-01
影响因子：
8.7
通讯作者：
Holt, CM
中科院分区：
文献类型：
--
作者：
Galea, J;Armstrong, J;Holt, CM
已知白介素1β(IL-1β)对冠状动脉内存在的不同类型的细胞有许多影响。在这项研究中，我们确定了人冠状动脉标本中含有IL-1β的细胞的位置和表型，并将IL-1β的存在与疾病严重程度联系起来。对管腔内皮细胞、外膜血管壁细胞和巨噬细胞进行免疫组织化学双重标记，以检测IL-1β蛋白和针对内皮细胞或巨噬细胞的细胞类型特异性单抗。用原位杂交法检测冠脉壁内IL-1βmRNA的表达。在这项研究中，与非缺血性心肌病心脏的冠状动脉相比，动脉粥样硬化性冠状动脉的外膜血管壁中IL-1β蛋白增加。这一增加与冠状动脉粥样硬化的严重程度成正比。在动脉粥样硬化的冠状动脉和非缺血心肌病的冠状动脉的管腔内皮细胞和巨噬细胞中也检测到IL-1β蛋白。IL-1β表达于管腔内皮细胞、外膜血管内皮细胞和巨噬细胞。我们的结论是，IL-1β是由缺血心脏的冠状动脉内皮细胞和巨噬细胞产生的，在较小程度上来自非缺血性心肌病心脏。
Interleukin-1 beta (IL-1 beta) is known to have a number of effects on the different cell types present within coronary arteries. In this study we identified the location and phenotype of cells containing IL-1 beta in human coronary artery specimens from patients suffering from either coronary atherosclerosis or cardiomyopathy and correlated the presence of IL-1 beta with disease severity. Luminal endothelial cells, adventitial vessel wall cells, and macrophages were double labeled immunohistochemically for IL-1 beta protein and a cell type-specific monoclonal antibody for either endothelial cells or macrophages. In situ hybridization was performed to locate the presence of IL-1 beta mRNA within the coronary artery wall. In this study IL-1 beta protein was found to be increased in the adventitial vessel walls of atherosclerotic coronary arteries compared with coronary arteries from nonischemic cardiomyopathic hearts. This increase was directly proportional to the severity of coronary atherosclerosis. IL-1 beta protein was also detected in luminal endothelium and macrophages of atherosclerotic coronary arteries and coronary arteries from nonischemic cardiomyopathic hearts. IL-1 beta mRNA was found in luminal endothelial cells, adventitial vessel endothelial cells, and macrophages. We conclude that IL-1 beta is produced by endothelial cells and macrophages in coronary arteries from ischemic hearts and to a lesser extent from nonischemic cardiomyopathic hearts.