doi: 10.1161/01.ATV.0000172686.16863.be
© 2005 American Heart Association, Inc.
Editorials |
Down But Not Out
New Insights Into the Role of 
Vß3 Integrins in Vascular Healing
From the Division of Cardiology (G.A.S.) and Carolina Cardiovascular Biology Center (G.A.S., A.P., R.Z., J.H.), University of North Carolina, Chapel Hill, NC.
Correspondence to George A. Stouffer, MD, Division of Cardiology, University of North Carolina, Chapel Hill, NC 27599-7075. E-mail rstouff@med.unc.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Integrins are heterodimeric transmembrane glycoproteins involved in cell-cell and cell-extracellular matrix interactions. Two highly homologous ß3-containing integrins have been identified: vß3 (also known as the vitronectin receptor) and IIbß3 (also known as platelet glycoprotein [GP] IIb/IIIa). vß3 can be expressed by a variety of cell types including endothelial cells, smooth muscle cells (SMCs), leukocytes, platelets, osteoclasts, and mesangial cells, whereas IIbß3 is found only on platelets and megakaryocytes. vß3 consists of a 125-kDa subunit and a 105-kDa ß subunit and, in addition to vitronectin, binds other extracellular proteins including osteopontin, fibronectin, fibrinogen, thrombospondin, proteolysed collagen, DEL1 (developmentally regulated endothelial locus-1), plasminogen activator inhibitor (PAI)-1, prothrombin, DANCE (developmental arteries and neural crest epidermal growth factor [EGF]-like), and von Willebrand factor (vWF). Similar to IIbß3 integrins on platelets, vß3 integrins exist in active and inactive conformations, with variable affinity for ligands, depending on the cell type and modulation by signaling events.1
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In the normal artery, vascular expression of vß3 integrins is generally limited to the luminal endothelial monolayer.2,3 After vascular injury, vß3 expression increases markedly, a finding that has been consistent across numerous animal models including baboons, rats, rabbits, mice, and pigs.4 vß3 expression is observed rapidly in the media after injury and is found in the neointima within 7 days, with peak levels at 14 to 28 days.2–7 vß3 integrin expression colocalizes with -actin in the injured arteries, suggesting that SMCs within the vessel wall express vß3 integrins after vascular injury.2,7 Recently, Sadeghi et al, using an 111
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