Evidence map›Paper›PMID 22173746›Full record

ArticleDigestive diseases and sciences2012

Osteopontin ablation attenuates progression of colitis in TNBS model.

Helieh S Oz, Jian Zhong, Willem J S de Villiers

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Digestive diseases and sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Colon Expression of Chemokines and Their Receptors Depending on the Stage ofInternational journal of molecular sciences · 2022
    Article
  3. Nutrients · 2021
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Osteopontin in Immune-mediated Diseases.Journal of dental research · 2015
    Review
  11. Article
  12. Osteopontin expression by CD103- dendritic cells drives intestinal inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  13. Article
  14. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Helieh S OzDepartment of Physiology, University of Kentucky Medical Center, Lexington, KY 40515-0298, USA. Hoz2@email.uky.edu
Jian Zhong
Willem J S de Villiers
University of Kentucky · US

Funding

Green Tea Polyphenols: A Novel Approach to IBDR21AT001490 · NCCIH · UNIVERSITY OF KENTUCKY · PI OZ, HELIEH S · 2004 to 2005
$365k
A Novel Murine Model of Chronic Inflammatory PeriodontitusR03DE019177 · NIDCR · UNIVERSITY OF KENTUCKY · PI OZ, HELIEH S · 2009 to 2010
$223k
NCCIH NIH HHS AT1490NIDCR NIH HHS DE19177
6 · The paper itself

Abstract

introductionOPN has been implicated in the inflammatory response to Crohn's disease. We hypothesized that OPN deficiency protects against different stages of TNBS-induced colitis in a modified model that mimics Crohn's disease. MATERIAL AND

methodsOPN-deficient and wildtype mice were treated intracolonically with TNBS and euthanized during acute, sub-acute and chronic colitis.

resultsTNBS-treated wildtype mice developed severe colitis, but OPN-deficient mice were significantly protected. Wildtype mice showed significant infiltration of inflammatory cells including macrophages, and colonic transmural thickening that progressed to strictures, increased matrix collagen deposits (X2 fold), and granuloma formation. These pathological findings were partially attenuated by OPN deficiency. The inflammatory marker, serum amyloid A (SAA), markedly increased in sub-acute stages regardless of OPN status. Conversely, OPN deficiency significantly reduced concentration of SAA in the acute and chronic stages. Secretory OPN was upregulated particularly in acute stage in wildtypes (P < 0.001) and as expected not present in OPN-deficient animals. Flow cytometry analysis of splenic macrophages revealed significant increases in scavenger receptors, macrosialin and F4/80 markers' expression in wildtypes.

conclusionsOur data support the role of OPN in induction of inflammation and establishment of chronic colitis. Therefore, OPN may represent a target for therapeutic intervention in Crohn's disease.

Indexed as

AnimalsBiopsy, NeedleColitisDisease Models, AnimalDisease ProgressionFlow CytometryImmunohistochemistryInflammation MediatorsMaleMiceMice, Inbred C57BLMice, KnockoutOsteopontinRandom AllocationReference ValuesSensitivity and SpecificityInflammation MediatorsOsteopontinSerum Amyloid A ProteinTrinitrobenzenesulfonic Acid

Identifiers

PMID22173746
OpenAlexW1997940422

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.