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- W1012649247 abstract "Atherosclerosis is an inflammatory disease initiated by hyperlipidemia and monocyte recruitment. Low shear stress and cytokine activation increases VCAM-1 expression, the principle endothelial receptor facilitating monocyte arrest. We reported that monocyte integrin CD11c/CD18 binds VCAM-1 and cooperates with VLA-4 to arrest monocytes on inflamed endothelium. In this study, we determined if CD11c expression on monocytes from 60 human donors increased in a hyperlipidemic state. Blood was drawn from fasting donors and again at 3.5hrs after a 45% fat meal. Resting and MCP-1 stimulated levels of CD11c on monocytes were increased after the meal. Highest CD11c expression correlated with high blood levels of total cholesterol (>200mg/dL) and low HDL (<35mg/dL). To assess the role of CD11c in recruitment, monocytes were isolated from ApoE−/−/CD11c−/− mice and perfused through a microfluidic chamber derivatized with VCAM-1 and E-selectin. When CD11c was absent there was a 45% decrease in firm arrest compared to CD11c+/+ cells. Antibody blocking of VLA-4 inhibited monocyte arrest to a similar extent for both genotypes. When firmly arrested monocytes were exposed to a 5-fold increase in shear stress, 40% more CD11c+/+ cells remained firmly arrested. We conclude hyperlipidemia associated with a high fat meal can upregulate monocyte CD11c, and its binding to VCAM-1 is a critical step in high avidity monocyte adhesion. Research supported by HL082689 to S.I.S. and T32 HL086350-01A1 to R.M.G." @default.
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- W1012649247 date "2009-04-01" @default.
- W1012649247 modified "2023-09-26" @default.
- W1012649247 title "Monocyte CD11c/CD18 expression is upregulated postprandially and mediates firm arrest on VCAM‐1" @default.
- W1012649247 doi "https://doi.org/10.1096/fasebj.23.1_supplement.640.5" @default.
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