Expression of syndecan-1 in inflammatory bowel disease and a possible mechanism of heparin therapy

Heparin apparently aids healing in ulcerative colitis although its mechanis m of action is unknown. The purpose of this study was to investigate the hy pothesis that heparin functions as a coreceptor molecule for basic fibrobla st growth factor, a role usually performed by heparan sulfate chains on syn decan-1, A marked reduction of syndecan-1 immunostaining was found in repar ative epithelium from inflammatory bowel disease patients. Removal of hepar an sulfate on gastrointestinal epithelial cells in vitro reduced the prolif erative response to basic fibroblast growth factor. The response to basic f ibroblast growth factor was completely restored by the addition of heparin, Loss of syndecan-1 expression occurs in the regenerative mucosa in inflamm atory bowel disease. Although this may facilitate tissue motility, its loss probably adversely affects the ability of cells to bind basic fibroblast g rowth factor. The present data show that heparin may substitute the loss of functional activity of syndecan-1 in the binding of basic fibroblast growt h factor.