Evidence map›Paper›PMID 24286264›Full record

ArticleBritish journal of pharmacology2014

Role of the A(2B) receptor-adenosine deaminase complex in colonic dysmotility associated with bowel inflammation in rats.

L Antonioli, M Fornai, O Awwad, G Giustarini, C Pellegrini, M Tuccori, V Caputi, M Qesari, I Castagliuolo, P Brun and 4 more

Open access · greenAbstract read
In one paragraph

Article in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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.

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

16 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Adenosine Signaling in Autoimmune Disorders.Pharmaceuticals (Basel, Switzerland) · 2020
    Review
  6. Article
  7. Review
  8. Article
  9. Emerging Role of Purine Metabolizing Enzymes in Brain Function and Tumors.International journal of molecular sciences · 2018
    Review
  10. Article
  11. Article
  12. Adenosine AJournal of clinical medicine · 2017
    Review
  13. Article
  14. Article
  15. Article
  16. 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

14 authors at 3 institutions in 1 country.

L AntonioliDivision of Pharmacology and Chemotherapy, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
M Fornai
O Awwad
G Giustarini
C Pellegrini
M Tuccori
V Caputi
M Qesari
I Castagliuolo
P Brun
M C Giron
C Scarpignato
C Blandizzi
R Colucci
University of Pisa · ITUniversity of Padua · ITUniversity of Parma · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeAdenosine A(2B) receptors regulate several physiological enteric functions. However, their role in the pathophysiology of intestinal dysmotility associated with inflammation has not been elucidated. Hence, we investigated the expression of A2B receptors in rat colon and their role in the control of cholinergic motility in the presence of bowel inflammation. EXPERIMENTAL APPROACH: Colitis was induced by 2,4-dinitrobenzenesulfonic acid (DNBS). Colonic A(2B) receptor expression and localization were examined by RT-PCR and immunofluorescence. The interaction between A(2B) receptors and adenosine deaminase was assayed by immunoprecipitation. The role of A(2B) receptors in the control of colonic motility was examined in functional experiments on longitudinal muscle preparations (LMPs). KEY

resultsA(2B) receptor mRNA was present in colon from both normal and DNBS-treated rats but levels were increased in the latter. A(2B) receptors were predominantly located in the neuromuscular layer, but, in the presence of colitis, were increased mainly in longitudinal muscle. Functionally, the A(2B) receptor antagonist MRS 1754 enhanced both electrically-evoked and carbachol-induced cholinergic contractions in normal LMPs, but was less effective in inflamed tissues. The A(2B) receptor agonist NECA decreased colonic cholinergic motility, with increased efficacy in inflamed LMP. Immunoprecipitation and functional tests revealed a link between A(2B) receptors and adenosine deaminase, which colocalize in the neuromuscular compartment. CONCLUSIONS AND IMPLICATIONS: Under normal conditions, endogenous adenosine modulates colonic motility via A2B receptors located in the neuromuscular compartment. In the presence of colitis, this inhibitory control is impaired due to a link between A2B receptors and adenosine deaminase, which catabolizes adenosine, thus preventing A(2B) receptor activation.

Indexed as

AdenineAdenosine DeaminaseAdenosine Deaminase InhibitorsAnimalsBenzenesulfonatesColitisColonGastrointestinal MotilityIn Vitro TechniquesMaleMuscle ContractionMuscle, SmoothPeroxidaseRatsRats, Sprague-DawleyReceptor, Adenosine A2B2,4-dinitrobenzenesulfonic acid9-(2-hydroxy-3-nonyl)adenineAdenineAdenosine DeaminaseAdenosine Deaminase InhibitorsBenzenesulfonatesPeroxidaseReceptor, Adenosine A2BTumor Necrosis Factor-alphaA2B receptoradenosinecolitiscolonic neuromuscular contractions

Identifiers

PMID24286264
PMCPMC3952807
OpenAlexW1522255132

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.