The role of junctional adhesion molecules in vascular inflammation

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Abstract
Junctional adhesion molecules (JAMs) are expressed by leukocytes, platelets, endothelial and epithelial cells. JAMs are important in the control of vascular permeability and leukocyte transmigration across endothelial-cell surfaces. JAMs engage in homophilic interactions and various heterophilic interactions with the leukocyte integrins lymphocyte function-associated antigen 1 (LFA1), very late antigen 4 (VLA4) and MAC1. JAMs are upregulated under inflammatory, atherosclerotic or ischaemic conditions. JAMs are redistributed from intercellular junctions to the cell surface after inflammatory stimulation. Both endothelial-cell and leukocyte JAM-A contribute in a molecular 'zipper' that controls transendothelial diapedesis, whereas JAM-C supports leukocyte adhesion on platelets and subsequent transendothelial migration. Both JAM-A and JAM-C promote leukocyte recruitment on activated endothelium under inflammatory conditions. Studies using genetically modified mice have shown important roles for JAMs in the regulation of leukocyte recruitment to sites of inflammation, ischaemia–reperfusion injury, atherogenesis, and in neointima formation. JAMs are involved in growth-factor-mediated angiogenesis by association with αvβ3-integrin and subsequent signalling steps.

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