Evidence map›Paper›PMID 22621785›Full record

ArticleAmerican journal of physiology. Cell physiology2012

Soluble epoxide hydrolase expression in a porcine model of arteriovenous graft stenosis and anti-inflammatory effects of a soluble epoxide hydrolase inhibitor.

William G Sanders, Christophe Morisseau, Bruce D Hammock, Alfred K Cheung, Christi M Terry

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. Soluble Epoxide Hydrolase Inhibition byInternational journal of molecular sciences · 2020
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Autologous fat transplants to deliver glitazone and adiponectin for vasculoprotection.Journal of controlled release : official journal of the Controlled Release Society · 2017
    Article
  9. Article
  10. Article
  11. Article
  12. The role of epoxyeicosatrienoic acids in the cardiovascular system.British journal of clinical pharmacology · 2015
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Novel therapies for hemodialysis vascular access dysfunction: myth or reality?Clinical journal of the American Society of Nephrology : CJASN · 2013
    Review
  19. 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.

William G SandersDepartment of Pharmaceutics, University of Utah, Salt Lake City, Utah 84112, USA.
Christophe Morisseau
Bruce D Hammock
Alfred K Cheung
Christi M Terry
University of Utah · USUniversity of California, Davis · US

Funding

PREVENTION OF HEMODIALYSIS VASCULAR ACCESS STENOSISR01HL067646 · NHLBI · UNIVERSITY OF UTAH · PI CHEUNG, ALFRED K · 2002 to 2010
$8.0M
NHLBI NIH HHS R01 HL067646NHLBI NIH HHS R01HL-67646
6 · The paper itself

Abstract

Synthetic arteriovenous (AV) grafts, placed between an artery and vein, are used for hemodialysis but often fail due to stenosis, typically at the vein-graft anastomosis. This study recorded T lymphocyte and macrophage accumulation at the vein-graft anastomosis, suggesting a role for inflammation in stenosis development. Epoxyeicosatrienoic acids (EETs), products of cytochrome P-450 epoxidation of arachidonic acid, have vasculoprotective and anti-inflammatory effects including inhibition of platelet activation, cell migration, and adhesion. EETs are hydrolyzed by soluble epoxide hydrolase (sEH) to less active diols. The effects of a specific inhibitor of sEH (sEHI) on cytokine release from human monocytes and mouse bone marrow-derived macrophages (BMMΦ) from wild-type (WT) and sEH knockout (KO) animals were investigated. Expression of sEH protein increased over time at the anastomosis as evaluated by immunohistochemistry. Pre-exposure of adherent human monocytes to sEHI (5 μM) significantly inhibited lipopolysaccharide-induced release of monocyte chemotactic protein-1 (MCP-1) and tumor necrosis factor-α and enhanced the EET-to-diol ratio. Release of MCP-1 from WT BMMΦ was significantly inhibited but release from sEH KO BMMΦ was not attenuated indicating the specificity of the sEHI. In contrast, sEHI did not inhibit the release of macrophage inflammatory protein-1 or interleukin-6. Nuclear translocation of NF-κB, as assessed by immunocytochemical staining, was not decreased with sEHI in monocytes, but the phosphorylation of JNK was completely abrogated, suggesting this pathway is the target of sEHI effects in monocytes. These results suggest that sEHI may be useful for inhibition of inflammation and subsequently stenosis in AV grafts.

Indexed as

AnimalsAnti-Inflammatory AgentsArteriovenous Shunt, SurgicalBenzoatesCells, CulturedChemokine CCL2CytokinesDisease Models, AnimalEicosanoidsEnzyme InhibitorsEpoxide HydrolasesGraft Occlusion, VascularHumansLipopolysaccharidesMacrophagesMice4-(4-(3-(4-trifluoromethoxy-phenyl)ureido)cyclohexyloxy)benzoic acidAnti-Inflammatory AgentsBenzoatesCCL2 protein, humanChemokine CCL2CytokinesEicosanoidsEnzyme InhibitorsEpoxide HydrolasesLipopolysaccharidesPhenylurea CompoundsTumor Necrosis Factor-alpha

Identifiers

PMID22621785
PMCPMC3423029
OpenAlexW2114149686

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.