Digestive Diseases and Sciences

, Volume 44, Issue 12, pp 2508–2515 | Cite as

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

Abstract

Heparin apparently aids healing in ulcerativecolitis although its mechanism of action is unknown. Thepurpose of this study was to investigate the hypothesisthat heparin functions as a coreceptor molecule for basic fibroblast growth factor, a roleusually performed by heparan sulfate chains onsyndecan-1. A marked reduction of syndecan-1immunostaining was found in reparative epithelium frominflammatory bowel disease patients. Removal of heparansulfate on gastrointestinal epithelial cells in vitroreduced the proliferative response to basic fibroblastgrowth factor. The response to basic fibroblast growth factor was completely restored by the additionof heparin. Loss of syndecan-1 expression occurs in theregenerative mucosa in inflammatory bowel disease.Although this may facilitate tissue motility, its loss probably adversely affects the ability ofcells to bind basic fibroblast growth factor. Thepresent data show that heparin may substitute the lossof functional activity of syndecan-1 in the binding of basic fibroblast growth factor.

SYNDECAN HEPARIN INFLAMMATORY BOWEL DISEASE 

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Copyright information

© Plenum Publishing Corporation 1999

Authors and Affiliations

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

There are no affiliations available

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