Evidence map›Paper›PMID 21737340›Full record

ArticleOral oncology2011

Role of AMP-18 in oral mucositis.

Peili Chen, Mark Lingen, Stephen T Sonis, Margaret M Walsh-Reitz, F Gary Toback

Abstract read
In one paragraph

Article in Oral oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. The pathogenesis of mucositis: updated perspectives and emerging targets.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2019
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. The role of gastrokine 1 in gastric cancer.Journal of gastric cancer · 2014
    Review
  10. Article
  11. Emerging evidence on the pathobiology of mucositis.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2013
    Review
  12. Article
  13. Emerging evidence on the pathobiology of mucositis.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2013
    Review
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 2 institutions in 1 country.

Peili ChenDepartment of Medicine, University of Chicago, Chicago, IL 60637, United States.
Mark Lingen
Stephen T Sonis
Margaret M Walsh-Reitz
F Gary Toback
University of Chicago · USBrigham and Women's Hospital · US

Funding

Targeting Tight Junctions To Treat MucositisR21DE018811 · NIDCR · UNIVERSITY OF CHICAGO · PI TOBACK, FREDERICK GARY · 2009 to 2010
$429k
NIDCR NIH HHS R21 DE018811
6 · The paper itself

Abstract

Oral mucositis (OM) is a devasting toxicity associated with cytotoxic cancer therapy. Antrum mucosal protein (AMP)-18 and a synthetic peptide surrogate, exhibit cell protective and mitogenic properties in in vitro and in vivo models of gastrointestinal epithelial cell injury. The mucosal barrier-protective effects may be mediated by AMP-18's capacity to increase accumulation of specific tight junction (TJ) and adherens junction proteins, and also protect against their loss after injury. Here we asked if AMP peptide could protect the oral mucosa and speed healing from radiation-induced injury. We found AMP peptide prevented radiation-induced OM in a murine model. The peptide also stimulated HaCaT cell growth used to model the oral mucosa. Binding of recombinant human (rh) AMP-18 to the plasma membrane of keratinocytes in normal human oral mucosal tissue suggested that its effects may be receptor mediated. Using an immobilized His-tagged rhAMP-18 fusion protein the receptor was identified as the cholecystokinin-B/gastrin receptor (CCKBR) by affinity purification and mass spectrometry analysis. CCKBR was expressed and co-immunoprecipitated with exogenous rhAMP-18 in diverse epithelial cell lines. Immunofluorescence staining revealed that rhAMP-18 colocalized with CCKBR on the surface of CCKBR-transfected cells. Furthermore, rhAMP-18-stimulated signaling pathways were blocked by a CCKBR-specific antagonist, YM022. rhAMP-18 enhanced viability and growth of CCKBR-transfected, but not empty vector-transfected cells. These results suggest the importance of epithelial junctional integrity in the pathogenesis of OM and demonstrate that AMP-18, by targeting TJ proteins through the activation of CCKBR, could provide a novel strategy for the prevention and treatment of OM.

Indexed as

Adherens JunctionsAnimalsBenzodiazepinesDisease Models, AnimalFemaleFluorescent Antibody TechniqueHumansKeratinocytesMass SpectrometryMiceMucous MembranePeptide HormonesReceptor, Cholecystokinin BRecombinant ProteinsStomatitisTight JunctionsBenzodiazepinesGKN1 protein, humanPeptide HormonesReceptor, Cholecystokinin BRecombinant ProteinsYM 022

Identifiers

PMID21737340
PMCPMC3164219
OpenAlexW2003074628

What OpenQuestion holds

Textmetadata
LicenceTDM
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.