Evidence map›Paper›PMID 26197453›Full record

ArticleInflammatory bowel diseases2015

Antrum Mucosal Protein-18 Peptide Targets Tight Junctions to Protect and Heal Barrier Structure and Function in Models of Inflammatory Bowel Disease.

Peili Chen, Danika Bakke, Lauren Kolodziej, James Lodolce, Christopher R Weber, David L Boone, F Gary Toback

Open access · bronzeAbstract read
In one paragraph

Article in Inflammatory bowel diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 26 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Peili ChenDepartment of Medicine, University of Chicago, Chicago, Illinois.
Danika BakkeDepartment of Medicine, University of Chicago, Chicago, Illinois.
Lauren KolodziejDepartment of Medicine, University of Chicago, Chicago, Illinois.
James LodolceDepartment of Medicine, University of Chicago, Chicago, Illinois.
Christopher R WeberDepartment of Pathology, University of Chicago, Chicago, Illinois.
David L BooneDepartment of Medicine, Indiana University School of Medicine, South Bend, Indiana.
F Gary TobackThe University of Chicago, Department of Medicine, MC5100, 5841 South Maryland, Avenue, Chicago, IL.
University of Chicago · USIndiana University · US

Funding

Re-Engineering Translational Research at the University of ChicagoUL1TR000430 · NCATS · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2012 to 2016
$20.2M
Mechanisms and pathways of trans-tight junction conductanceK08DK088953 · NIDDK · UNIVERSITY OF CHICAGO · PI WEBER, CHRISTOPHER · 2010 to 2014
$733k
A Novel Agent with Dual Functions to Treat Head and Neck CancerR21CA176032 · NCI · UNIVERSITY OF CHICAGO · PI TOBACK, FREDERICK GARY · 2014 to 2015
$378k
Mechanisms of tight junction pore and leak pathway regulation in intestinal mucosR03DK103007 · NIDDK · UNIVERSITY OF CHICAGO · PI WEBER, CHRISTOPHER · 2014 to 2015
$158k
NCATS NIH HHS UL1 TR000430NCI NIH HHS R21 CA176032NIDDK NIH HHS K08 DK088953NIDDK NIH HHS R03 DK103007PHS HHS R21 NCI 176032
6 · The paper itself

Abstract

backgroundA peptide derived from Antrum Mucosal Protein (AMP)-18 (gastrokine-1) reduces the extent of mucosal erosions and clinical severity in mice with dextran sulfate sodium-induced colonic injury. This study set out to determine if AMP peptide was also therapeutic for immune- and cytokine-mediated mouse models of intestinal injury and inflammatory bowel diseases by enhancing and stabilizing tight junctions.

methodsTherapeutic effects of AMP peptide were examined in interleukin-10-deficient and a T-cell adoptive transfer models of colitis in immunodeficient recombinase activating gene-1 knock-out (RAG-1-/-) mice. Mechanisms by which AMP peptide enhances barrier function and structure were studied ex vivo using intestine and colon from mice given lipopolysaccharide and in AMP-18-deficient mice given dextran sulfate sodium.

resultsIn interleukin-10-deficient mice given piroxicam, AMP peptide enhanced recovery after weight loss, protected against colon shortening and segmental dilation, and reduced the colitis activity score. In the T-cell transfer model, treatment with the peptide protected against colon shortening. In mice given lipopolysaccharide in vivo to induce gut injury, AMP peptide prevented the onset of, and reversed established intestinal hyperpermeability by targeting TJ proteins and perijunctional actin. AMP-18-deficient mice challenged with dextran sulfate sodium exhibited increased mortality, developed erosions in the colon, and had lower levels of ZO-1 in TJs than heterozygous littermates or wild-type mice.

conclusionsThe results indicate that AMP-18/peptide may serve a protective role against injury along the gastrointestinal mucosal barrier, and recommend further development of AMP peptide as a novel agent to treat patients with inflammatory bowel disease.

Indexed as

ActinsAdoptive TransferAnimalsAnti-Inflammatory Agents, Non-SteroidalColitisColonCytokinesDextran SulfateInterleukin-10LipopolysaccharidesMiceMice, Inbred C57BLMice, KnockoutModels, AnimalPeptide HormonesPermeabilityActinsAnti-Inflammatory Agents, Non-SteroidalCytokinesDextran SulfateGKN1 protein, humanInterleukin-10LipopolysaccharidesPeptide HormonesPiroxicamProtective AgentsTight Junction Proteins

Identifiers

PMID26197453
PMCPMC4567513
OpenAlexW996226864

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.