Coronary artery endothelial cells and microparticles increase expression of VCAM-1 in myocardial infarction.
Coronary artery endothelial cells and microparticles increase expression of VCAM-1 in myocardial infarction.
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DOI：
10.1160/th14-02-0151
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发表时间：
2015-03
影响因子：
6.7
通讯作者：
Armstrong EJ
中科院分区：
文献类型：
--
作者：
Radecke CE;Warrick AE;Singh GD;Rogers JH;Simon SI;Armstrong EJ
冠状动脉疾病（CAD）的特点是进行性动脉粥样硬化斑块导致血流限制性狭窄，而心肌梗死（MI）是由于斑块破裂或侵蚀并导致冠状动脉突然闭塞而发生。多种炎症途径影响斑块稳定性，但对冠状动脉狭窄部位内皮炎症的直接评估很大程度上仅限于病理样本或动脉粥样硬化动物模型。我们描述了一种在球囊血管成形术和经皮冠状动脉介入治疗期间直接从冠状动脉斑块部位分离和表征内皮细胞 (EC) 和 EC 微粒 (EMP) 的技术。使用成像流式细胞术 (IFC) 鉴定冠状动脉内皮细胞 (CAEC)，并在血管成形术后立即评估个体 CAEC 和促动脉粥样硬化粘附分子血管细胞粘附分子 1 (VCAM-1) 的 EMP 表达。与稳定 CAD 患者相比，MI 患者的 CAEC 上的 VCAM-1 表达量高出 73%，EMP 上的表达量高出 79%。相比之下，来自这些相同受试者的外周循环中的 EC 上不存在 VCAM-1 表达。 MI 患者 CAEC 和 EMP 上的 VCAM-1 密度显着较高，并且与心肌梗死面积标志物呈正相关。我们得出的结论是，心肌梗塞患者 EC 上 VCAM-1 表达的增加以及冠状动脉斑块部位 EMP 的形成与血管炎症程度呈正相关。
Coronary artery disease (CAD) is characterised by progressive atherosclerotic plaque leading to flow-limiting stenosis, while myocardial infarction (MI) occurs due to plaque rupture or erosion with abrupt coronary artery occlusion. Multiple inflammatory pathways influence plaque stability, but direct assessment of endothelial inflammation at the site of coronary artery stenosis has largely been limited to pathology samples or animal models of atherosclerosis. We describe a technique for isolating and characterising endothelial cells (ECs) and EC microparticles (EMPs) derived directly from the site of coronary artery plaque during balloon angioplasty and percutaneous coronary intervention. Coronary artery endothelial cells (CAECs) were identified using imaging flow cytometry (IFC), and individual CAEC and EMP expression of the pro-atherogenic adhesion molecule vascular cell adhesion molecule-1 (VCAM-1) was assessed immediately following angioplasty. Patients with MI registered 73 % higher VCAM-1 expression on their CAECs and 79 % higher expression on EMPs compared to patients with stable CAD. In contrast, VCAM-1 expression was absent on ECs in the peripheral circulation from these same subjects. VCAM-1 density was significantly higher on CAECs and EMPs among patients with MI and positively correlated with markers of myocardial infarct size. We conclude that increased VCAM-1 expression on EC and formation of EMP at the site of coronary plaque is positively correlated with the extent of vascular inflammation in patients with myocardial infarction.