High levels of IsoDGR-modified fibronectin are associated with higher levels of macrophages and other rupture-prone plaque characteristics in patients undergoing carotid endarterectomy

Abstract

Objective Deamidation of the NGR (Asn-Gly-Arg) motif to the isoDGR (isoAsp-Gly-Arg) motif in fibronectin (IsoDGR-fibronectin) enhances in vitro monocyte and endothelial cell activation. Blocking isoDGR reduces macrophage influx in murine tissues. Although macrophage influx is an important feature of human plaque destabilization, the role for plasma and plaque isoDGR-fibronectin in macrophage influx in the atherosclerotic plaque and thereby increasing plaque vulnerability has not been investigated in large human cohorts.