Evidence map›Paper›PMID 19808663›Full record

ArticleThe Journal of biological chemistry2009

Nrf2-dependent and -independent responses to nitro-fatty acids in human endothelial cells: identification of heat shock response as the major pathway activated by nitro-oleic acid.

Emilia Kansanen, Henna-Kaisa Jyrkkänen, Oscar L Volger, Hanna Leinonen, Annukka M Kivelä, Sanna-Kaisa Häkkinen, Steven R Woodcock, Francisco J Schopfer, Anton J Horrevoets, Seppo Ylä-Herttuala and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

101 citing papers in PubMed, 163 citations in OpenAlex.

  1. Trial
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  11. Lipoxin AbioRxiv : the preprint server for biology · 2024
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Nitro Fatty Acids (NOMolecules (Basel, Switzerland) · 2021
    Review
  18. Review
  19. Article
  20. Review

41 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

12 authors at 3 institutions in 3 countries.

Emilia KansanenDepartment of Biotechnology and Molecular Medicine, A. I. Virtanen Institute for Molecular Sciences, University of Kuopio, FIN-70211 Kuopio, Finland.
Henna-Kaisa Jyrkkänen
Oscar L Volger
Hanna Leinonen
Annukka M Kivelä
Sanna-Kaisa Häkkinen
Steven R Woodcock
Francisco J Schopfer
Anton J Horrevoets
Seppo Ylä-Herttuala
Bruce A Freeman
Anna-Liisa Levonen
University of Eastern Finland · FIUniversity of Pittsburgh · USAmsterdam UMC Location VUmc · NL

Funding

Redox-Derived Pulmonary Anti-Inflammatory MediatorsR01HL064937 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FREEMAN, BRUCE ALAN · 2000 to 2015
$5.6M
NITRIC OXIDE REGULATION OF VASCULAR OXIDANT INJURYR01HL058115 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FREEMAN, BRUCE ALAN · 1998 to 2007
$3.3M
NHLBI NIH HHS R01 HL058115NHLBI NIH HHS R01 HL064937NHLBI NIH HHS R01 HL58115NHLBI NIH HHS R01 HL64937
6 · The paper itself

Abstract

Electrophilic fatty acid derivatives, including nitrolinoleic acid and nitro-oleic acid (OA-NO(2)), can mediate anti-inflammatory and pro-survival signaling reactions. The transcription factor Nrf2, activated by electrophilic fatty acids, suppresses redox-sensitive pro-inflammatory gene expression and protects against vascular endothelial oxidative injury. It was therefore postulated that activation of Nrf2 by OA-NO(2) accounts in part for its anti-inflammatory actions, motivating the characterization of Nrf2-dependent and -independent effects of OA-NO(2) on gene expression using genome-wide transcriptional profiling. Control and Nrf2-small interfering RNA-transfected human endothelial cells were treated with vehicle, oleic acid, or OA-NO(2), and differential gene expression profiles were determined. Although OA-NO(2) significantly induced the expression of Nrf2-dependent genes, including heme oxygenase-1 and glutamate-cysteine ligase modifier subunit, the majority of OA-NO(2)-regulated genes were regulated by Nrf2-independent pathways. Moreover, gene set enrichment analysis revealed that the heat shock response is the major pathway activated by OA-NO(2), with robust induction of a number of heat shock genes regulated by the heat shock transcription factor. Inasmuch as the heat shock response mediates anti-inflammatory and cytoprotective actions, this mechanism is proposed to contribute to the protective cell signaling functions of nitro-fatty acids and other electrophilic fatty acid derivatives.

Indexed as

Blotting, WesternCell LineCells, CulturedCluster AnalysisDose-Response Relationship, DrugEndothelial CellsGene ExpressionGene Expression ProfilingGlutamate-Cysteine LigaseHeme Oxygenase-1Hot TemperatureHumansLinoleic AcidsNAD(P)H Dehydrogenase (Quinone)NF-E2-Related Factor 2Nitro Compounds10-nitro-9,12-octadecadienoic acidGCLM protein, humanGlutamate-Cysteine LigaseHeme Oxygenase-1HMOX1 protein, humanLinoleic AcidsNAD(P)H Dehydrogenase (Quinone)NFE2L2 protein, humanNF-E2-Related Factor 2Nitro CompoundsNQO1 protein, humanOleic Acids

Identifiers

PMID19808663
PMCPMC2785166
OpenAlexW2109621677

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.