New Member of Endothelial Arsenal Against Inflammation
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The endothelium evolved from a conceptual cellophane-like structure involved in blood–tissue exchange of solutes to an active set of vascular cells with a diverse and broad array of functions in health and disease.1,2 Because of its strategic immediate contact with blood and tissues, the endothelium regulates transport barrier properties, contributes to control of blood flow, prevents hemorrhage through fine tuning of platelet adhesion, and is an important player in controlling immunologic responses. Several articles and reviews have pointed out that endothelial dysfunction is the fundamental basis of inflammation and vascular disease.3–6
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Research in vascular biology has identified several key endothelial proteins along with factors that cause the onset of inflammation. Tissue necrosis factor-α is a major cytokine that activates endothelial cells and promotes inflammation. Proteins involved in regulatory functions include intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and vascular endothelial cadherin. Intercellular adhesion molecule-1-1 and vascular cell adhesion molecule-1-1 play an important role in adhesion and migration of leukocytes in inflammation,7 whereas vascular endothelial cadherin participates in the regulation of microvascular transport.8,9
The proteins mentioned in the preceding paragraph, as well as the proteins that serve as coagulation factors, are largely located on the cell membrane and exert their main function by reacting to external stimuli. Interest in the biology of endothelial cells was immensely enhanced by the realization that they produce endogenous factors, …