on October 7, 2004
Published online before print October 7, 2004, doi: 10.1161/01.ATV.0000147163.54024.70
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Submitted on August 12, 2004
Accepted on September 27, 2004
Molecular Interactions Leading to Lipoprotein Retention and the Initiation of Atherosclerosis
Maged F. Khalil ;
From the Division of Preventive Medicine & Nutrition (M.F.K., I.J.G.), Columbia University College of Physicians & Surgeons, New York, NY; and the Department of Pathology (W.D.W.), Wake Forest University School of Medicine, Winston-Salem, NC.
* To whom correspondence should be addressed. E-mail: ijg3{at}columbia.edu.
Abstract--Atherosclerosis is distinguished by the accumulation of lipoprotein lipid within the arterial wall. An ionic interaction of positively charged regions of apolipoprotein (apo) B with matrix proteins, including proteoglycans, collagen, and fibronectin, is thought to initiate this process. Proteoglycans are complex glycoproteins containing highly negatively charged carbohydrate chains. These proteins are abundant in atherosclerosis lesions, and they associate with apoB-containing lipoproteins. Several specific regions of apoB may mediate this process. Other lipoprotein-associated proteins, including apoE and lipases, might also participate in this process. In addition, retention may occur via lipoprotein association with other matrix molecules or as a consequence of intra-arterial lipoprotein aggregation.
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