Evidence map›Paper›PMID 11481030›Full record

ArticleBMC gastroenterology2001

TNF-alpha induced endothelial MAdCAM-1 expression is regulated by exogenous, not endogenous nitric oxide.

T Oshima, P Jordan, M B Grisham, J S Alexander, M Jennings, M Sasaki, K Manas

Open access · goldAbstract read
In one paragraph

Article in BMC gastroenterology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.6field-weighted citation impact, top 36% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Observational
  2. Review
  3. Article
  4. Article
  5. Review
  6. CC16 Binding to αAmerican journal of respiratory and critical care medicine · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Role of the endothelium in inflammatory bowel diseases.World journal of gastroenterology · 2011
    Review
  12. Article
  13. Article
  14. Role of MutS homolog 2 (MSH2) in intestinal myofibroblast proliferation during Crohn's disease stricture formation.American journal of physiology. Gastrointestinal and liver physiology · 2008
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

7 authors at 1 institution in 1 country.

T OshimaDepartment of Molecular and Cellular Physiology, Louisiana State University Health Science Center, Shreveport, Louisiana, USA. toshim@lsumc.edu
P Jordan
M B Grisham
J S Alexander
M Jennings
M Sasaki
K Manas
Louisiana State University Health Sciences Center Shreveport · US

Funding

VASCULAR REACTIVITY FOLLOWING ISCHEMIA-REPERFUSIONP01DK043785 · NIDDK · LOUISIANA STATE UNIV HSC SHREVEPORT · PI GRANGER, D. NEIL · 1991 to 2011
$17.0M
LUNG ENDOTHELIAL JUNCTION PROTEINSR29HL047615 · NHLBI · VANDERBILT UNIVERSITY · PI ALEXANDER, JONATHAN STEVEN · 1994 to 1997
–
NHLBI NIH HHS HL47615NIDDK NIH HHS DK43785NIDDK NIH HHS DK47663NIDDK NIH HHS P01 DK043785
6 · The paper itself

Abstract

backgroundMAdCAM-1 is an adhesion molecule expressed in Peyer's patches and lymphoid tissues which is mobilized by cytokines like TNF-alpha and is a major determinant of lymphocyte trafficking to the gut in human inflammatory bowel disease (IBD). It has been suggested that both reactive oxygen and nitrogen metabolites participate in regulating adhesion molecule expression in response to TNF-alpha.

methodsTo examine how exogenous and endogenous sources of NO modulate MAdCAM-1 induction by TNF-alpha, we pre-treated mouse lymphatic endothelial cells with either long or short acting NO donors prior to TNF-alpha-stimulation, and measured MAdCAM-1 induction at 24 h. RESULTS AND DISCUSSION: DETA-NO, a long-acting NO donor, and SperNO, a rapid releasing NO donor both inhibited TNF-alpha-stimulated MAdCAM-1 expression in a concentration dependent manner. Both NO donors also reduced a4b7-dependent lymphocyte endothelial adhesion. Inhibition of endogenous NO production by either L-NAME, a non-selective NOS inhibitor, or by 1400 w, a selective iNOS inhibitor failed to induce, or potentiate TNF-alpha regulated MAdCAM-1 expression.

conclusionsExogenous NO donors may be beneficial in the treatment of IBD, while endogenous nitric oxide synthases may be less effective in controlling adhesion molecule expression in response to cytokines.

Indexed as

AmidinesAnimalsBenzylaminesCD8-Positive T-LymphocytesCell AdhesionCell Adhesion MoleculesCell LineEndotheliumImmunoblottingImmunoglobulinsInflammatory Bowel DiseasesMiceMucoproteinsNitric OxideNitric Oxide DonorsNitric Oxide Synthase1-hydroxy-2-oxo-3,3-bis(2-aminoethyl)-1-triazeneAmidinesBenzylaminesCell Adhesion MoleculesImmunoglobulinsMADCAM1 protein, humanMadcam1 protein, mouseMucoproteinsN-(3-(aminomethyl)benzyl)acetamidineNitric OxideNitric Oxide DonorsNitric Oxide SynthaseNitrogen OxidesSperminespermine nitric oxide complexTriazenesTumor Necrosis Factor-alpha

Identifiers

PMID11481030
PMCPMC35355
OpenAlexW1518156951

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.