Evidence map›Paper›PMID 15545995›Full record

ArticleThe Journal of clinical investigation2004

A role for proteinase-activated receptor-1 in inflammatory bowel diseases.

Nathalie Vergnolle, Laurie Cellars, Andrea Mencarelli, Giovanni Rizzo, Sunita Swaminathan, Paul Beck, Martin Steinhoff, Patricia Andrade-Gordon, Nigel W Bunnett, Morley D Hollenberg and 3 more

RetractedOpen access · bronzeAbstract readComparative StudyRetracted Publication
In one paragraph

Article in The Journal of clinical investigation, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
5.7field-weighted citation impact, top 3% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 97 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Targeting PAR1: Now What?Trends in pharmacological sciences · 2017
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. The protein C pathway and pathologic processes.Journal of thrombosis and haemostasis : JTH · 2009
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 5 institutions in 4 countries.

Nathalie VergnolleDepartment of Pharmacology and Therapeutics, University of Calgary, Calgary, Alberta, Canada. nvergnol@ucalgary.ca
Laurie Cellars
Andrea Mencarelli
Giovanni Rizzo
Sunita Swaminathan
Paul Beck
Martin Steinhoff
Patricia Andrade-Gordon
Nigel W Bunnett
Morley D Hollenberg
John L Wallace
Giuseppe Cirino
Stefano Fiorucci
University of Calgary · CAUniversity of Perugia · ITJohnson & Johnson (United States) · USUniversity of Münster · DEUniversity of Naples Federico II · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Proteinase-activated receptor-1 (PAR1), a G protein-coupled receptor activated by thrombin, is highly expressed in different cell types of the gastrointestinal tract. The activity of thrombin and of other proteinases is significantly increased in the colon of inflammatory bowel disease (IBD) patients. Since PAR1 activation in tissues other than the gut provoked inflammation, we hypothesized that PAR1 activation in the colon is involved in the pathogenesis of IBD. Here, we demonstrate that PAR1 is overexpressed in the colon of IBD patients. In mice, intracolonic administration of PAR1 agonists led to an inflammatory reaction characterized by edema and granulocyte infiltration. This PAR1 activation-induced inflammation was dependent on B and T lymphocytes. Moreover, PAR1 activation exacerbated and prolonged inflammation in a mouse model of IBD induced by the intracolonic administration of trinitrobenzene sulfonic acid (TNBS), while PAR1 antagonism significantly decreased the mortality and severity of colonic inflammation induced by TNBS and dextran sodium sulfate. In these 2 models, colitis development was strongly attenuated by PAR1 deficiency. Taken together, these results imply an important role for PAR1 in the pathogenesis of experimental colitis, supporting the notion that PAR1 inhibition may be beneficial in the context of IBD and possibly in other chronic intestinal inflammatory disorders.

Indexed as

AdultAnimalsB-LymphocytesColitisColonDextran SulfateDisease Models, AnimalDose-Response Relationship, DrugFemaleHumansImmunohistochemistryInflammatory Bowel DiseasesIntestinal MucosaKineticsMaleMiceDextran SulfatePeptide FragmentsPeroxidaseReceptor, PAR-1RNA, MessengerThrombinTrinitrobenzenesulfonic Acid

Identifiers

PMID15545995
PMCPMC526028
OpenAlexW2127625135

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.