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Overview
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Background
CD29 (β1 integrin subunit, GPIIa) forms non-covalently linked heterodimers with at least 6 different α chains (α1-α6, CD49a-f) determining the binding properties of β1 (VLA) integrins. These integrins mediate cell adhesion to collagen, fibronectin, laminin and other extracellular matrix (ECM) components. This interaction hinders cell death, whereas disruption of anchorage to ECM leads to apoptosis. Decreased expression of most β1 integrins correlates with acquiring multidrug resistance of tumor cells during selection in presence of antitumor drug. In platelets, translocation of intracellular pool of β1 integrins to the plasma membrane following thrombin stimulation. These integrins are also up-regulated in leukocytes during emigration and extravascular migration and appear to be critically involved in regulating the immune cell trafficking from blood to tissue, as well as in regulating tissue damage and disease symptoms related to inflammatory bowel disease. Through a β1 integrin-dependent mechanism, fibronectin and type I collagen enhance cytokine secretion of human airway smooth muscle in response to IL-1β.
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