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(Circulation Research. 2007;100:450.)
© 2007 American Heart Association, Inc.

Editorials

G Protein–Coupled Receptor G2A

Friend or Foe of the Vasculature?

Kaikobad Irani

From the Cardiovascular Institute, University of Pittsburgh, Pa.

Correspondence to Dr Kaikobad Irani, Associate Professor, University of Pittsburgh, Cardiovascular Institute, Scaife S620, 3550 Terrace St., Pittsburgh, PA 15261. E-mail iranik@upmc.edu

See related article, pages 572–580

Key Words: atherosclerosis • inflammation • endothelium

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

Atherosclerosis is, in large part, an inflammatory process. White blood cells of different lineages are essential components of the atherosclerotic plaque. More important than their numbers, white blood cells influence the structure of an atherosclerotic plaque, and the function of the vessel in which the plaque is present, by secreting a host of agents that affect resident vascular cells.¹

Macrophages, derived from circulating monocytes, are one class of white blood cells that, as part of the atherosclerotic plaque, play a critical part in the progression of the plaque, and in compromising its structural integrity.¹ Long before an atherosclerotic plaque is clinically detectable, one of the earliest steps in its genesis is the adhesion of circulating monocytes to the endothelium, and subsequent transmigration into the vessel wall. Because it is well-recognized that these very early stages are critical to plaque development, a great deal of energy has been devoted to trying to understand the mechanisms underpinning them.

The work by Hedrick and colleagues in this issue of Circulation Research² adds to this understanding. This work examines the part of a G protein–coupled receptor, G2A, in modulating the interaction between monocytes and the vascular endothelium. Using mice that are deficient for G2A, the authors convincingly demonstrate that endogenous G2A tonically inhibits accumulation of monocytes in the vascular wall. G2A is abundantly expressed in hematopoietic cells (including monocytes), and has been shown to inhibit proliferation of lymphoid cells.³ However, with transplants of bone marrows of G2A-deficient and wild-type mice into -irradiated wild-type and . . . [Full Text of this Article]