Evidence map›Paper›PMID 21666111›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2011

Antecedent hydrogen sulfide elicits an anti-inflammatory phenotype in postischemic murine small intestine: role of heme oxygenase-1.

Mozow Y Zuidema, Kelly J Peyton, William P Fay, William Durante, Ronald J Korthuis

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
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

25 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. InactivatedExperimental and therapeutic medicine · 2020
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Preconditioning with the BKAmerican journal of physiology. Heart and circulatory physiology · 2017
    Article
  12. Hydrogen sulfide improves intestinal recovery following ischemia by endothelial nitric oxide-dependent mechanisms.American journal of physiology. Gastrointestinal and liver physiology · 2017
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  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

5 authors.

Mozow Y ZuidemaDepartment of Medical Pharmacology and Physiology, University of Missouri-Columbia School of Medicine, Columbia, Missouri 65212, USA.
Kelly J Peyton
William P Fay
William Durante
Ronald J Korthuis

Funding

CARBON MONOXIDE AND VASCULAR SMOOTH MUSCLE CELL FUNCTIONR01HL059976 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI DURANTE, WILLIAM · 1999 to 2013
$3.3M
Ethanol Prevents Microvascular DysfunctionR01AA014945 · NIAAA · UNIVERSITY OF MISSOURI-COLUMBIA · PI KORTHUIS, RONALD JOHN · 2006 to 2010
$1.6M
NHLBI NIH HHS HL-059976NHLBI NIH HHS R01 HL059976NIAAA NIH HHS AA-014945
6 · The paper itself

Abstract

We recently demonstrated that preconditioning with an exogenous hydrogen sulfide donor (NaHS-PC) 24 h before ischemia and reperfusion (I/R) causes postcapillary venules to shift to an anti-inflammatory phenotype in C57BL/6J wild-type (WT) mice such that these vessels fail to support increases in postischemic leukocyte rolling (LR) and leukocyte adhesion (LA). The objective of the present study was to determine whether heme oxygenase-1 (HO-1) is a mediator of these anti-inflammatory effects noted during I/R in mice preconditioned with NaHS. Intravital fluorescence microscopy was used to visualize LR and LA in single postcapillary venules of the murine small intestine. I/R induced marked increases in LR and LA, effects that were prevented by NaHS-PC. Treatment with the HO inhibitor tin protoporphyrin IX, but not the inactive protoporphyrin CuPPIX, just before reperfusion prevented the anti-inflammatory effects of antecedent NaHS. The anti-inflammatory effects of NaHS-PC were mimicked by preconditioning with hemin, an agent that induces HO-1 expression. We then evaluated the effect of NaHS as a preconditioning stimulus in mice that were genetically deficient in HO-1 (HO-1(-/-) on an H129 background with appropriate WT strain controls). NaHS-PC was ineffective in HO-1(-/-) mice. Our work indicates that HO-1 serves as an effector of the anti-inflammatory effects of NaHS-PC during I/R 24 h later.

Indexed as

Analysis of VarianceAnimalsAnti-Inflammatory AgentsCell AdhesionDisease Models, AnimalDose-Response Relationship, DrugEndothelial CellsEnzyme InhibitorsHeme Oxygenase-1Hydrogen SulfideIntestine, SmallLeukocyte RollingMaleMembrane ProteinsMetalloporphyrinsMiceAnti-Inflammatory AgentsEnzyme InhibitorsHeme Oxygenase-1Hmox1 protein, mouseHydrogen SulfideMembrane ProteinsMetalloporphyrinsProtoporphyrinssodium bisulfideSulfidestin protoporphyrin IX

Identifiers

PMID21666111
PMCPMC3191101

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.