doi: 10.1161/ATVBAHA.109.195552
© 2009 American Heart Association, Inc.
Editorials |
Tyrosine Sulfation of Leukocyte Adhesion Molecules and Chemokine Receptors Promotes Atherosclerosis
From the Division of Inflammation Biology, La Jolla Institute for Allergy & Immunology, Calif.
Correspondence to Klaus Ley, MD, Division of Inflammation Biology, La Jolla Institute for Allergy & Immunology, 9420 Athena Circle Drive, La Jolla, CA 92037. E-mail klaus@liai.org
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Westmuckett and Moore describe a prominent role of tyrosine sulfation in hematopoietic cells during atherosclerosis development.1 Atherosclerosis represents a major health problem in developed and developing countries and is the most common underlying process precipitating myocardial infarctions, limb ischemia, and stroke. In the United States alone, more than 60 million people have some form of atherosclerotic vascular disease.2 Atherosclerosis is a complex disease associated with lipid accumulation and formation of atherosclerotic plaque in the major arteries of the body, which can rupture or erode to cause acute thrombosis, arterial occlusion, and necrosis of the dependent tissue.
See accompanying article on page 1730
In a last two decades, it has become clear that immune processes play an important role in atherosclerosis development, plaque formation, and progression of the disease. Although all major types of immune cells are involved in atherosclerosis (reviewed in3), the exact molecular and cellular mechanisms of disease development and progression are not completely understood. Two commonly used mouse models of atherosclerosis are apolipoprotein E-deficient Apoe–/– or low-density lipoprotein (LDL) receptor-deficient Ldlr–/– mice. In both models, LDL cholesterol is elevated, which promotes atherosclerotic lesion formation in locations similar to those in the human disease. Ldlr–/– mice can be reconstituted with bone marrow from donor mice to produce chimeric mice lacking targeted molecules of interest in hematopoietic cells only.
Leukocyte recruitment is critical for chronic inflammation and progression of atherosclerosis. This process is regulated by adhesion molecules and chemoattractants
Related Article:
Arterioscler Thromb Vasc Biol 2009 29: 1730-1736.