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Arteriosclerosis, Thrombosis, and Vascular Biology
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Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:1890-1891
doi: 10.1161/ATVBAHA.108.173575
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:1890.)
© 2008 American Heart Association, Inc.


Editorials

Antiinflammatory Actions of HDL

A New Insight

Kerry-Anne Rye; Philip J. Barter

From the Lipid Research Group (K.-A.R., P.J.B.), The Heart Research Institute, Sydney; the Faculty of Medicine (K.-A.R., P.J.B.), University of Sydney; and the Department of Medicine (K.-A.R.), University of Melbourne, Australia.

Correspondence to K.-A. Rye, PhD, Lipid Research Group, The Heart Research Institute, 114 Pyrmont Bridge Road, Camperdown, Sydney, New South Wales, Australia, 2050. E-mail ryek@hri.org.au or karye@ozemail.com.au


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

Atherosclerosis is an inflammatory disorder characterized by the accumulation of macrophages and T-lymphocytes in the arterial intima. The macrophages are derived from blood monocytes that adhere to, and transmigrate across, an activated or injured endothelial surface. The firm adhesion of monocytes to the endothelium requires expression of integrins such as CD11/CD18 on the monocyte surface and endothelial expression of the adhesion molecules vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin. Monocytes that are firmly tethered to the endothelium transmigrate into the subendothelial space in a process that is dependent on endothelial expression of chemokines such as monocyte chemotactic protein-1 (MCP-1).1

See accompanying article on page 2071

After entering the artery wall, monocytes differentiate into macrophages in processes that are mediated by macrophage colony stimulating factor (CSF) and granulocyte-macrophage CSF.2 Macrophages express a range of scavenger receptors that bind and internalize modified LDL in an unregulated manner. This leads to a progressive accumulation of lipids in the macrophages and the formation of foam cells: the hallmark cells of atherosclerotic lesions.

The results of numerous epidemiological studies have established that high density lipoprotein (HDL) levels correlate inversely with the risk of developing cardiovascular disease.3 This relationship reflects several functions of HDL, the most extensively studied of which is their ability to remove excess cholesterol from cells, such as macrophages in the artery wall, in the first step of the reverse cholesterol transport pathway.4 In addition to their lipid transporting properties, HDL have antioxidant and antithrombotic properties.5,6 They are also . . . [Full Text of this Article]


Related Article:

High-Density Lipoprotein Reduces the Human Monocyte Inflammatory Response
Andrew J. Murphy, Kevin J. Woollard, Anh Hoang, Nigora Mukhamedova, Roslynn A. Stirzaker, Sally P.A. McCormick, Alan T. Remaley, Dmitri Sviridov, and Jaye Chin-Dusting
Arterioscler Thromb Vasc Biol 2008 28: 2071-2077. [Abstract] [Full Text] [PDF]



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