Evidence map›Paper›PMID 27866158›Full record

ArticleThe Journal of biological chemistry2016

A Nitric Oxide Storage and Transport System That Protects Activated Macrophages from Endogenous Nitric Oxide Cytotoxicity.

Hiu Chuen Lok, Sumit Sahni, Patric J Jansson, Zaklina Kovacevic, Clare L Hawkins, Des R Richardson

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
4.5field-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

15 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Glutathione-Biomolecules · 2022
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  5. Expressed Soybean Leghemoglobin: Effect onMolecules (Basel, Switzerland) · 2021
    Article
  6. The Relationship of Glutathione-Molecules (Basel, Switzerland) · 2021
    Review
  7. Review
  8. Article
  9. Review
  10. A mononuclear nonheme {FeNO}Chemical science · 2018
    Article
  11. Biochemistry of proinflammatory macrophage activation.Cellular and molecular life sciences : CMLS · 2018
    Review
  12. Article
  13. Review
  14. Article
  15. Genetic and Dietary Iron Overload Differentially Affect the Course ofFrontiers in cellular and infection microbiology · 2017
    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

6 authors at 3 institutions in 1 country.

Hiu Chuen LokFrom the Molecular Pharmacology and Pathology Program, Department of Pathology and Bosch Institute, University of Sydney, Sydney, New South Wales 2006 and.
Sumit SahniFrom the Molecular Pharmacology and Pathology Program, Department of Pathology and Bosch Institute, University of Sydney, Sydney, New South Wales 2006 and.
Patric J JanssonFrom the Molecular Pharmacology and Pathology Program, Department of Pathology and Bosch Institute, University of Sydney, Sydney, New South Wales 2006 and.
Zaklina KovacevicFrom the Molecular Pharmacology and Pathology Program, Department of Pathology and Bosch Institute, University of Sydney, Sydney, New South Wales 2006 and.
Clare L Hawkinsthe Heart Research Institute, Sydney, New South Wales 2042, Australia.
Des R RichardsonFrom the Molecular Pharmacology and Pathology Program, Department of Pathology and Bosch Institute, University of Sydney, Sydney, New South Wales 2006 and d.richardson@med.usyd.edu.au.
University of Sydney · AURobert Bosch (Australia) · AUThe Heart Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nitric oxide (NO) is integral to macrophage cytotoxicity against tumors due to its ability to induce iron release from cancer cells. However, the mechanism for how activated macrophages protect themselves from endogenous NO remains unknown. We previously demonstrated by using tumor cells that glutathione S-transferase P1 (GSTP1) sequesters NO as dinitrosyl-dithiol iron complexes (DNICs) and inhibits NO-mediated iron release from cells via the transporter multidrug resistance protein 1 (MRP1/ABCC1). These prior studies also showed that MRP1 and GSTP1 protect tumor cells against NO cytotoxicity, which parallels their roles in defending cancer cells from cytotoxic drugs. Considering this, and because GSTP1 and MRP1 are up-regulated during macrophage activation, this investigation examined whether this NO storage/transport system protects macrophages against endogenous NO cytotoxicity in two well characterized macrophage cell types (J774 and RAW 264.7). MRP1 expression markedly increased upon macrophage activation, and the role of MRP1 in NO-induced

Indexed as

AnimalsATP-Binding Cassette, Sub-Family C ProteinsBiological TransportBronchodilator AgentsCells, CulturedGlutathioneGlutathione S-Transferase piIron IsotopesMacrophage ActivationMacrophagesMiceMice, KnockoutNitric OxidePropionatesProtective AgentsQuinolinesATP-Binding Cassette, Sub-Family C ProteinsBronchodilator AgentsGlutathioneGlutathione S-Transferase piGstp1 protein, mouseGstp2 protein, mouseIron Isotopesmultidrug resistance-associated protein 1Nitric OxidePropionatesProtective AgentsQuinolinesRNA, Small Interferingverlukastelectron paramagnetic resonance (EPR)macrophagenitric oxidenitric oxide synthasetumor

Identifiers

PMID27866158
PMCPMC5207136
OpenAlexW2551089624

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.