Review |
From Vascular Science (R.M.R.), National Heart and Lung Institute, Imperial College School of Medicine, Hammersmith Hospital, London, UK; and Center for Excellence in Vascular Biology (L.Y., G.G.-C., F.W.L.), Department of Pathology, Brigham and Womens Hospital and Harvard Medical School, Boston, Mass.
Correspondence to Francis W. Luscinskas, Brigham and Womens Hospital, 77 Ave Louis Pasteur, NRB 7 Rm 752, Boston, MA 02115. E-mail fluscinskas{at}rics.bwh.harvard.edu
This Review is part of a thematic series on Migration of Vascular Cells, which includes the following articles:
Mechanisms of Vascular Smooth Muscle Cell Migration
Endothelial Cell Migration During Angiogenesis
Endothelial Precursor Cell Migration During Vasculogenesis
Endothelial-Dependent Mechanisms of Leukocyte Recruitment to the Vascular Wall
Molecular Mechanisms of Endothelial Cell Migration
Kathy K. Griendling Editor
Inflammation is a fundamental process that protects organisms by removing or neutralizing injurious agents. A key event in the inflammatory response is the localized recruitment of various leukocyte subsets. Here we address the cellular and regulatory mechanisms of leukocyte recruitment to the vessel wall in cardiovascular disease and discuss our evolving understanding of the role of the vascular endothelium in this process. The vascular endothelium is the continuous single-cell lining of the cardiovascular system that forms a critical interface between the blood and its components on one side and the tissues and organs on the other. It is heterogeneous and has many synthetic and metabolic functions including secretion of platelet-derived growth factor, von Willebrand factor, prostacyclin, NO, endothelin-1, and chemokines and the expression of adhesion molecules. It also acts as a nonthrombogenic and selective permeable barrier. Endothelial cells also interact closely with the extracellular matrix and with adjacent cells including pericytes and smooth muscle cells within the vessel wall. A central question in vascular biology is the role of the endothelium in the initiation of inflammatory response, the extent of its "molecular conversations" with recruited leukocytes, and its influence on the extent and/or outcome of this response.
Key Words: inflammation monocyte lymphocytes atherogenesis adhesion molecules
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