Adhesion molecules in scleroderma: collagen binding integrins
Abstract
In summary, adhesion molecules are likely to play a prominent role in scleroderma pathogenesis and evolution. Endothelial adhesion molecules required for leukocyte extravasation are upregulated in affected tissue, though the mechanism is unclear. Certainly, endothelial adhesion molecule expression is seen in the context of other diseases not characterized by fibrosis. Adhesion molecules on the fibroblast, particularly those that play a role in fibroblast collagen interactions, may be very important. The ability of fibroblasts to organize collagen fibrils, and to exert forces across collagenous tissue, is likely to involve a prominent role of alpha 2 beta 1 integrin. Enhanced organization and contraction of newly formed collagen, as well as unregulated procollagen production, may be intimately linked in this disease process. At least two factors that strongly enhance fibroblast force generation could potentially influence other aspects of scleroderma. TGF beta is a potent stimulus for collagen production and has been found to be elevated in lesional scleroderma. Endothelin 1 is also a potent vasoconstrictor and is elevated in scleroderma patient serum as well [60,62-65]. Its apparent role in other fibrocontractive diseases sugge...Continue Reading
References
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Adhesion Molecules in Health and Disease
Cell adhesion molecules are a subset of cell adhesion proteins located on the cell surface involved in binding with other cells or with the extracellular matrix in the process called cell adhesion. In essence, cell adhesion molecules help cells stick to each other and to their surroundings. Cell adhesion is a crucial component in maintaining tissue structure and function. Discover the latest research on adhesion molecule and their role in health and disease here.