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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:1748.)
© 2004 American Heart Association, Inc.

Editorials

Vascular Cross-Talk: A Conversation

Margarete Mehrabian; Hooman Allayee

From the Department of Medicine (M.M.), David Geffen School of Medicine at UCLA, and the Department of Preventive Medicine and Institute for Genetic Medicine (H.A.), USC Keck School of Medicine, Los Angeles, Calif.

Correspondence to Margarete Mehrabian, UCLA School of Medicine, Department of Medicine/Division of Cardiology, Los Angeles, CA 90024. E-mail mmehrabi@ucla.edu

An extract of the first 250 words of the full text is provided, because this article has no 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

View larger version (29K): [in this window] [in a new window]   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 ß1 (Itgb1, VLA4) and ß2 (CD11b) integrins on monocytes. The ß1 and ß2 integrins bind to their cognate receptors, vascular cell adhesion molecule and intracellular adhesion molecule, firmly arresting monocytes on the endothelium. Binding of LTB4 to BLT1/2 on monocytes and endothelial cells induces MCP1 expression, thereby initiating a looping mechanism through which LTB4 and MCP1 can further regulate monocyte adhesion, . . . [Full Text of this Article]