title: Coronary artery endothelial cells and microparticles increase expression of VCAM-1 in myocardial infarction.
abstract: 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.
authors.forename: Christopher E
authors.initials: CE
authors.lastname: Radecke
authors.forename: Alexandra E
authors.initials: AE
authors.lastname: Warrick
authors.forename: Gagan D
authors.initials: GD
authors.lastname: Singh
authors.forename: Jason H
authors.initials: JH
authors.lastname: Rogers
authors.affiliation: Scott I. Simon, Department of Biomedical Engineering, University of California at Davis, 451 East Health Sciences Drive, Davis, CA 95616, USA, Tel.: +1 530 752 0299, E-mail sisimon@ucdavis.edu.
authors.forename: Scott I
authors.initials: SI
authors.lastname: Simon
authors.forename: Ehrin J
authors.initials: EJ
authors.lastname: Armstrong
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D015906:Angioplasty, Balloon, Coronary; D015415:Biomarkers / Q000378:metabolism; D002469:Cell Separation / Q000379:methods; D055252:Cell-Derived Microparticles / Q000378:metabolism* / Q000473:pathology; D002478:Cells, Cultured; D003324:Coronary Artery Disease / Q000175:diagnosis / Q000378:metabolism* / Q000628:therapy; D003331:Coronary Vessels / Q000378:metabolism* / Q000473:pathology; D042783:Endothelial Cells / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000175:diagnosis / Q000378:metabolism* / Q000628:therapy; D058226:Plaque, Atherosclerotic; D012720:Severity of Illness Index; D015854:Up-Regulation; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism*
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D019010:Vascular Cell Adhesion Molecule-1
keywords: Acute myocardial infarction; VCAM-1; adhesion molecules; endothelial cells; inflammation; microparticles