On-chip phenotypic analysis of inflammatory monocytes in atherogenesis and myocardial infarction

• DOI: 10.1073/pnas.1300651110
• Publication Date: 2013-08-06T05:36:09Z
• Authors: Greg A. Foster; R. Michael Gower; Kimber L. Stanhope; Peter J. Havel; Scott I. Simon; Ehrin J. Armstrong
• Keywords: CD16; Monocyte; CD11c

Monocyte recruitment to inflamed arterial endothelium initiates plaque formation and drives progression of atherosclerosis. Three distinct monocyte subsets are detected in circulation (CD14 ++ CD16 − , CD14 + ), each may play roles during atherogenesis myocardial infarction. We studied a range subjects that included otherwise healthy patients with elevated serum triglyceride levels presenting acute Our objective was correlate an individual’s risk the activation state subset as function changes adhesion receptor expression using flow cytometric quantitation integrins l -selectin membrane expression. A microfluidic-based laboratory-on-a-chip developed quantify efficiency monocytes sheared whole blood on vascular cell molecule-1, while characterizing topography captured monocytes. adhered sevenfold higher than other subsets, infarction capture this double for subjects. In hypertriglyceridemia, increase attributable uptake triglyceride-rich lipoproteins subsequent signaling via Phospholipase C–dependent mechanism CD11c expression, very late antigen–4 function, integrin coclustering within focal adhesive sites molecule-1. summary, we introduce unique method quantifying subsets. These experiments reveal CD11c/CD18 is inducible whose correlates inflammatory at