Journal
TRENDS IN CARDIOVASCULAR MEDICINE
Volume 19, Issue 4, Pages 140-145Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tcm.2009.07.006
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Funding
- NCRR NIH HHS [P20 RR018758-020004, P20 RR018758] Funding Source: Medline
- NHLBI NIH HHS [P01 HL085607-010003, R01 HL080569, R01 HL078679, R01 HL080569-04, R01 HL078679-04, P01 HL085607] Funding Source: Medline
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR018758] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL085607, R01HL080569, R01HL078679] Funding Source: NIH RePORTER
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Leukocyte recruitment to the arterial vessel wall is the first step in the development of atherosclerotic lesions. Leukocyte homing in this event proceeds through a well-defined adhesion cascade, which includes tethering, rolling, adhesion, and transmigration. Selectins, including the P-, E-, and L-selectins, and their ligands mediate the initial tethering and rolling. Interactions between selectins and their ligands serve as a braking system to decelerate fast-flowing leukocytes from the central blood stream and enable them to adhere to and transmigrate underneath the activated endothelium. The best characterized ligand for selectins is P-selectin glycoprotein ligand-1, an extended homodimeric mucin on leukocytes that binds to all three selectins. Recent studies show that differential expression or glycosylation of P-selectin glycoprotein ligand-1 in different leukocytes mediates selective recruitment of different subsets of monocytes or lymphocytes to atherosclerotic arteries. (Trends Cardiovasc Med 2009; 19:140-145) (C) 2009, Elsevier Inc.
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