Evidence map›Paper›PMID 10630505›Full record

ArticleDigestive diseases and sciences1999

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

R Day, M Ilyas, P Daszak, I Talbot, A Forbes

Registry-linked trialAbstract read
PubMed Publisher
In one paragraph

Article in Digestive diseases and sciences, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01430039 (Syndecan-1 as a Surrogate Marker for Inflammatory Bowel Disease), which is not on this map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT01430039 completednot on this mapstarted 2011, after this paper: background citation

Syndecan-1 as a Surrogate Marker for Inflammatory Bowel Disease

TypeobservationalSponsorMeir Medical CenterRan2011 to 2015Enrolled42ConditionsInflammatory Bowel DiseasesArmsblood sample, Blood sample - venous blood 10 ml.
3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 64 citations in OpenAlex.

  1. Inflammatory bowel disease and extracellular matrix: when victim becomes double agent.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  2. Article
  3. American journal of physiology. Gastrointestinal and liver physiology · 2022
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Altered molecular pattern of mucosal healing in Crohn's disease fibrotic stenosis.World journal of gastrointestinal pathophysiology · 2013
    Article
  11. Article
  12. Versatile role of heparanase in inflammation.Matrix biology : journal of the International Society for Matrix Biology · 2013
    Review
  13. Review
  14. Heparanase enzyme in chronic inflammatory bowel disease and colon cancer.Cellular and molecular life sciences : CMLS · 2012
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

R DayAcademic Department of Gastroenterology, ICRF Colorectal Cancer Unit, St Mark's Hospital, Harrow, UK.
M Ilyas
P Daszak
I Talbot
A Forbes
Norwich University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

Cells, CulturedColitis, UlcerativeCrohn DiseaseEpithelial CellsFibroblast Growth Factor 2Heparan SulfateHeparinHumansInflammatory Bowel DiseasesIntestinal MucosaMembrane GlycoproteinsProteoglycansSyndecan-1SyndecansFibroblast Growth Factor 2Heparan SulfateHeparinMembrane GlycoproteinsProteoglycansSDC1 protein, humanSyndecan-1Syndecans

Identifiers

PMID10630505
OpenAlexW1581769603

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.