Evidence map›Paper›PMID 17135253›Full record

ArticleThe Journal of biological chemistry2007

Compensatory mechanism for homeostatic blood pressure regulation in Ephx2 gene-disrupted mice.

Ayala Luria, Steven M Weldon, Alisa K Kabcenell, Richard H Ingraham, Damian Matera, Huiping Jiang, Rajan Gill, Christophe Morisseau, John W Newman, Bruce D Hammock

Abstract read
In one paragraph

Article in The Journal of biological chemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing 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

80 citing papers in PubMed.

  1. Trial
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  12. Role of oxylipins in cardiovascular diseases.Acta pharmacologica Sinica · 2018
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

20 more citing papers are in PubMed but not listed here.

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

10 authors.

Ayala LuriaDepartment of Entomology, University of California, Davis, CA 95616, USA.
Steven M Weldon
Alisa K Kabcenell
Richard H Ingraham
Damian Matera
Huiping Jiang
Rajan Gill
Christophe Morisseau
John W Newman
Bruce D Hammock

Funding

Workshop on Environmental Technology Transfer and EntrepreneurshipP42ES004699 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 1987 to 2021
$50.1M
NIEHS Center for Health Effects of AgrochemicalsP30ES005707 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI MATSUMURA, FUMIO NONE · 1992 to 2006
$9.9M
HYDROLYTIC ENZYMES IN THE METABOLISM OF TOXINSR37ES002710 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 1998 to 2007
$3.0M
Metabolomic study of ozone and nitronaphthalene toxicityR01ES013933 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 2005 to 2009
$1.5M
NIEHS NIH HHS P30 ES005707NIEHS NIH HHS P30 ES05707NIEHS NIH HHS P42 ES004699NIEHS NIH HHS R01 ES013933NIEHS NIH HHS R37 ES002710NIEHS NIH HHS R37 ES02710
6 · The paper itself

Abstract

Arachidonic acid-derived epoxides, epoxyeicosatrienoic acids, are important regulators of vascular homeostasis and inflammation, and therefore manipulation of their levels is a potentially useful pharmacological strategy. Soluble epoxide hydrolase converts epoxyeicosatrienoic acids to their corresponding diols, dihydroxyeicosatrienoic acids, modifying or eliminating the function of these oxylipins. To better understand the phenotypic impact of Ephx2 disruption, two independently derived colonies of soluble epoxide hydrolase-null mice were compared. We examined this genotype evaluating protein expression, biofluid oxylipin profile, tissue oxylipin production capacity, and blood pressure. Ephx2 gene disruption eliminated soluble epoxide hydrolase protein expression and activity in liver, kidney, and heart from each colony. Plasma levels of epoxy fatty acids were increased, and fatty acid diols levels were decreased, while measured levels of lipoxygenase- and cyclooxygenase-dependent oxylipins were unchanged. Liver and kidney homogenates also show elevated epoxide fatty acids. However, in whole kidney homogenate a 4-fold increase in the formation of 20-hydroxyeicosatetraenoic acid was measured along with a 3-fold increase in lipoxygenase-derived hydroxylation and prostanoid production. Unlike previous reports, however, neither Ephx2-null colony showed alterations in basal blood pressure. Finally, the soluble epoxide hydrolase-null mice show a survival advantage following acute systemic inflammation. The data suggest that blood pressure homeostasis may be achieved by increasing production of the vasoconstrictor, 20-hydroxyeicosatetraenoic acid in the kidney of the Ephx2-null mice. This shift in renal metabolism is likely a metabolic compensation for the loss of the soluble epoxide hydrolase gene.

Indexed as

AnimalsBlood PressureCrosses, GeneticEpoxide HydrolasesEpoxy CompoundsExonsFatty Acids, NonesterifiedFemaleHomeostasisHumansKidneyLiverMaleMiceMice, Inbred C57BLMice, Inbred StrainsEphx2 protein, mouseEpoxide HydrolasesEpoxy CompoundsFatty Acids, Nonesterified

Identifiers

PMID17135253
PMCPMC2040337

What OpenQuestion holds

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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.