Vascular cross-talk: a conversation.

Abstract

The development of atherosclerotic lesions is a complex process that requires monocyte recruitment to the vascular endothelium. In response to oxidized lipid accumulation in the vessel wall, endothelial cells (ECs) express a series of chemokines and adhesion molecules that promote the recruitment and chemotaxis of monocyte/macrophages into the subendothelial space where they phagocytize oxidized lipids, forming foam cells and initiating processes leading to advanced lesions (Figure). Of the chemotactic molecules, monocyte chemotactic protein 1 (MCP1) is key in directing molecular signals essential for this process.1,2 However, little is know regarding the concerted actions of pathways and networks that coordinate this sequence of events. In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology , Huang and colleagues provide in vitro evidence for the involvement of the 5-lipoxygenase (5-LO) metabolite, leukotriene B4 (LTB4), and its receptors, BLT1 and 2, as critical players in monocyte chemotaxis and atherosclerosis.3 A model for LTB4 initiation of monocyte activation and recruitment. LTB4 regulates vascular monocyte chemotactic activity driven by MCP1, through the BLT1/2 signal transduction pathway. As monocytes tether onto endothelial cells, 5-lipoxygenase is induced, resulting in increased LTB4 production. This activates β1 (Itgb1, VLA4) and β2 …