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

Richard Day, Mohammad Ilyas, Peter Daszak, Ian Talbot, Alastair Forbes

Research output: Contribution to journalArticlepeer-review

51 Citations (Scopus)


Heparin apparently aids healing in ulcerative colitis although its mechanism of action is unknown. The purpose of this study was to investigate the hypothesis that heparin functions as a coreceptor molecule for basic fibroblast growth factor, a role usually performed by heparan sulfate chains on syndecan-1. A marked reduction of syndecan-1 immunostaining was found in reparative epithelium from inflammatory bowel disease patients. Removal of heparan sulfate on gastrointestinal epithelial cells in vitro reduced the proliferative response to basic fibroblast growth factor. The response to basic fibroblast growth factor was completely restored by the addition of heparin. Loss of syndecan-1 expression occurs in the regenerative mucosa in inflammatory bowel disease. Although this may facilitate tissue motility, its loss probably adversely affects the ability of cells to bind basic fibroblast growth factor. The present data show that heparin may substitute the loss of functional activity of syndecan-1 in the binding of basic fibroblast growth factor.
Original languageEnglish
Pages (from-to)2508-15
Number of pages8
JournalDigestive Diseases and Sciences
Issue number12
Publication statusPublished - Dec 1999


  • Cells, Cultured
  • Colitis, Ulcerative
  • Crohn Disease
  • Epithelial Cells
  • Fibroblast Growth Factor 2
  • Heparin
  • Heparitin Sulfate
  • Humans
  • Inflammatory Bowel Diseases
  • Intestinal Mucosa
  • Membrane Glycoproteins
  • Proteoglycans
  • Syndecan-1
  • Syndecans

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