Evidence map›Paper›PMID 22961094›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2013

Increased nuclear thioredoxin-1 potentiates cadmium-induced cytotoxicity.

Young-Mi Go, Michael Orr, Dean P Jones

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.2field-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

29 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
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  4. Article
  5. The Role of Thioredoxin System in Shank3 Mouse Model of Autism.Journal of molecular neuroscience : MN · 2024
    Article
  6. Article
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  10. Review
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  12. Review
  13. Low-Dose Cadmium Potentiates Metabolic Reprogramming Following Early-Life Respiratory Syncytial Virus Infection.Toxicological sciences : an official journal of the Society of Toxicology · 2022
    Article
  14. Article
  15. Article
  16. Article
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  19. Review
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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

3 authors at 1 institution in 1 country.

Young-Mi GoDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, Emory University, Atlanta, Georgia 30322, USA.
Michael Orr
Dean P Jones
Emory University · US

Funding

Metabolomics of subclinical and clinical cardiovascular diseaseP20HL113451 · NHLBI · EMORY UNIVERSITY · PI JONES, DEAN PAUL · 2012 to 2016
$4.3M
Thioredoxin-2 protection against mitochondrial oxidative toxicityR01ES009047 · NIEHS · EMORY UNIVERSITY · PI JONES, DEAN PAUL · 1998 to 2013
$3.9M
Nuclear and Cytoplasmic Redox in Oxidative StressR01ES011195 · NIEHS · EMORY UNIVERSITY · PI JONES, DEAN PAUL · 2001 to 2011
$3.3M
NHLBI NIH HHS P20 HL113451NIEHS NIH HHS ES009047NIEHS NIH HHS ES011195NIEHS NIH HHS R01 ES009047
6 · The paper itself

Abstract

Cadmium (Cd) is a widely dispersed environmental agent that causes oxidative toxicity through mechanisms that are sensitive to thioredoxin-1 (Trx1). Trx1 is a cytoplasmic protein that translocates to nuclei during oxidative stress. Recent research shows that interaction of Trx1 with actin plays a critical role in cell survival and that increased nuclear Trx-1 potentiates proinflammatory signaling and death in cell and mouse models. These observations indicate that oxidative toxicity caused by low-dose Cd could involve disruption of actin-Trx1 interaction, nuclear Trx1 translocation, and potentiation of proinflammatory cell death mechanisms. In this study, we investigated the role of nuclei-localized Trx1 in Cd-induced inflammation and cytotoxicity using in vitro and in vivo models. The results show that Cd stimulated nuclear translocation of Trx1 and p65 of NF-κB. Elevation of Trx1 in nuclei in in vitro cells and kidney of transgenic mice potentiated Cd-stimulated NF-κB activation and cell death. Cd-stimulated Trx1 nuclear translocation and NF-κB activation were inhibited by cytochalasin D, an inhibitor of actin polymerization, suggesting that actin regulates Trx1 nuclear translocation and NF-κB activation by Cd. A nuclear-targeted dominant negative form of Trx1 blocked Cd-stimulated NF-κB activation and decreased cell death. Addition of zinc, known to antagonize Cd toxicity by increasing metallothionein, had no effect on Cd-stimulated nuclear translocation of Trx1 and NF-κB activation. Taken together, the results show that nuclear translocation and accumulation of redox-active Trx1 in nuclei play an important role in Cd-induced inflammation and cell death.

Indexed as

AnimalsBlotting, WesternCadmiumCell Culture TechniquesCell NucleusCell SurvivalCysteineDose-Response Relationship, DrugElectrophoretic Mobility Shift AssayEnvironmental PollutantsGene ExpressionGlutathioneHeLa CellsHumansImmunohistochemistryMiceCadmiumCysteineEnvironmental PollutantsGlutathioneNF-kappa BNuclear Localization SignalsThioredoxinsTXN protein, human

Identifiers

PMID22961094
PMCPMC3621352
OpenAlexW2110914105

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.