Evidence map›Paper›PMID 19857569›Full record

ArticleFree radical biology & medicine2010

Activation of vascular endothelial nitric oxide synthase and heme oxygenase-1 expression by electrophilic nitro-fatty acids.

Nicholas K H Khoo, Volker Rudolph, Marsha P Cole, Franca Golin-Bisello, Francisco J Schopfer, Steven R Woodcock, Carlos Batthyany, Bruce A Freeman

Open access · greenAbstract readComparative Study
In one paragraph

Article in Free radical biology & medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.0field-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

44 citing papers in PubMed, 78 citations in OpenAlex.

  1. Review
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  7. Bioactive lipids in hypertension.Advances in pharmacology (San Diego, Calif.) · 2023
    Article
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  20. Nitrolipids in kidney physiology and disease.Nitric oxide : biology and chemistry · 2018
    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

8 authors at 3 institutions in 3 countries.

Nicholas K H KhooDepartment of Pharmacology and Chemical Biology, E1314 BST, University of Pittsburgh, Pittsburgh, PA 15261, USA. nkhoo@pitt.edu
Volker Rudolph
Marsha P Cole
Franca Golin-Bisello
Francisco J Schopfer
Steven R Woodcock
Carlos Batthyany
Bruce A Freeman
University of Pittsburgh · USInstitut Pasteur de Montevideo · UYUniversity Medical Center Hamburg-Eppendorf · DE

Funding

Redox-Derived Pulmonary Anti-Inflammatory MediatorsR01HL064937 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FREEMAN, BRUCE ALAN · 2000 to 2015
$5.6M
Redox Transduction of Nitric Oxide SignalingR37HL058115 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FREEMAN, BRUCE ALAN · 2008 to 2017
$5.2M
NITRIC OXIDE REGULATION OF VASCULAR OXIDANT INJURYR01HL058115 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FREEMAN, BRUCE ALAN · 1998 to 2007
$3.3M
Metabolic Stress-Induced Fatty Acid Nitration and Cardiovascular FunctionK99HL095769 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI COLE, MARSHA P · 2010 to 2011
$145k
NHLBI NIH HHS HL64937NHLBI NIH HHS HL8115NHLBI NIH HHS K99 HL095769NHLBI NIH HHS R01 HL058115NHLBI NIH HHS R01 HL064937NHLBI NIH HHS R37 HL058115
6 · The paper itself

Abstract

Reactive oxygen species mediate a decrease in nitric oxide (NO) bioavailability and endothelial dysfunction, with secondary oxidized and nitrated by-products of these reactions contributing to the pathogenesis of numerous vascular diseases. While oxidized lipids and lipoproteins exacerbate inflammatory reactions in the vasculature, in stark contrast the nitration of polyunsaturated fatty acids and complex lipids yields electrophilic products that exhibit pluripotent anti-inflammatory signaling capabilities acting via both cGMP-dependent and -independent mechanisms. Herein we report that nitro-oleic acid (OA-NO(2)) treatment increases expression of endothelial nitric oxide synthase (eNOS) and heme oxygenase 1 (HO-1) in the vasculature, thus transducing vascular protective effects associated with enhanced NO production. Administration of OA-NO(2) via osmotic pump results in a significant increase in eNOS and HO-1 mRNA in mouse aortas. Moreover, HPLC-MS/MS analysis showed that NO(2)-FAs are rapidly metabolized in cultured endothelial cells (ECs) and treatment with NO(2)-FAs stimulated the phosphorylation of eNOS at Ser(1179). These posttranslational modifications of eNOS, in concert with elevated eNOS gene expression, contributed to an increase in endothelial NO production. In aggregate, OA-NO(2)-induced eNOS and HO-1 expression by vascular cells can induce beneficial effects on endothelial function and provide a new strategy for treating various vascular inflammatory and hypertensive disorders.

Indexed as

AnimalsAorta, ThoracicCattleCells, CulturedCoronary VesselsEndothelium, VascularEnzyme ActivationHeme Oxygenase-1HumansHypertensionMaleMiceMice, Inbred C57BLNitric Oxide Synthase Type IIINitro CompoundsOleic AcidHeme Oxygenase-1Nitric Oxide Synthase Type IIINitro CompoundsOleic Acid

Identifiers

PMID19857569
PMCPMC2818734
OpenAlexW2063461543

What OpenQuestion holds

Textmetadata
LicenceTDM
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.