Evidence map›Paper›PMID 22521605›Full record

ArticleToxicology and applied pharmacology2012

Arsenite activates NFκB through induction of C-reactive protein.

Ingrid L Druwe, James J Sollome, Pablo Sanchez-Soria, Rhiannon N Hardwick, Todd D Camenisch, Richard R Vaillancourt

Open access · greenAbstract read
In one paragraph

Article in Toxicology and applied pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 12% 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, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Article
  6. Arsenic exposure and increasedRedox biochemistry and chemistry · 2023
    Article
  7. Devil's claw (Heliyon · 2020
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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

6 authors at 1 institution in 1 country.

Ingrid L DruweDepartment of Pharmacology & Toxicology, The University of Arizona College of Pharmacy, Tucson, AZ 85721, USA.
James J Sollome
Pablo Sanchez-Soria
Rhiannon N Hardwick
Todd D Camenisch
Richard R Vaillancourt
University of Arizona · US

Funding

TRANSPORT OF TRACE METALS IN A POLLUTED AQUIFERP42ES004940 · NIEHS · UNIVERSITY OF ARIZONA · PI Jon D Chorover · 1990 to 2026
$68.1M
SOUTHWEST ENVIRONMENTAL HEALTH SCIENCES CENTERP30ES006694 · NIEHS · UNIVERSITY OF ARIZONA · PI Nathan J Cherrington · 1994 to 2026
$36.7M
Training in Environmental Toxicology of Human DiseaseT32ES007091 · NIEHS · UNIVERSITY OF ARIZONA · PI Nathan J Cherrington · 1985 to 2026
$10.7M
The Role of Cytokine Signaling in Arsenic Induced Insulin ResistanceF31ES016990 · NIEHS · UNIVERSITY OF ARIZONA · PI DRUWE, INGRID · 2010 to 2010
$41k
NIEHS NIH HHS ES 006694NIEHS NIH HHS ES 016990NIEHS NIH HHS ES 04940NIEHS NIH HHS F31 ES016990NIEHS NIH HHS P30 ES006694NIEHS NIH HHS P42 ES004940NIEHS NIH HHS T32 ES007091
6 · The paper itself

Abstract

C-reactive protein (CRP) is an acute phase protein in humans. Elevated levels of CRP are produced in response to inflammatory cytokines and are associated with atherosclerosis, hypertension, cardiovascular disease and insulin resistance. Exposure to inorganic arsenic, a common environmental toxicant, also produces cardiovascular disorders, namely atherosclerosis and is associated with insulin-resistance. Inorganic arsenic has been shown to contribute to cardiac toxicities through production of reactive oxygen species (ROS) that result in the activation of NFκB. In this study we show that exposure of the hepatic cell line, HepG2, to environmentally relevant levels of arsenite (0.13 to 2 μM) results in elevated CRP expression and secretion. ROS analysis of the samples showed that a minimal amount of ROS are produced by HepG2 cells in response to these concentrations of arsenic. In addition, treatment of FvB mice with 100 ppb sodium arsenite in the drinking water for 6 months starting at weaning age resulted in dramatically higher levels of CRP in both the liver and inner medullary region of the kidney. Further, mouse Inner Medullary Collecting Duct cells (mIMCD-4), a mouse kidney cell line, were stimulated with 10 ng/ml CRP which resulted in activation of NFκB. Pretreatment with 10 nM Y27632, a known Rho-kinase inhibitor, prior to CRP exposure attenuated NFκB activation. These data suggest that arsenic causes the expression and secretion of CRP and that CRP activates NFκB through activation of the Rho-kinase pathway, thereby providing a novel pathway by which arsenic can contribute to metabolic syndrome and cardiovascular disease.

Indexed as

AmidesAnimalsArsenitesBiomarkersBiotransformationBlotting, WesternCell LineC-Reactive ProteinEnzyme-Linked Immunosorbent AssayFemaleHumansImmunohistochemistryKidneyLiverL-Lactate DehydrogenaseLuciferasesAmidesarseniteArsenitesBiomarkersC-Reactive ProteinL-Lactate DehydrogenaseLuciferasesNF-kappa BProtein Kinase InhibitorsPyridinesReactive Oxygen Speciesrho-Associated KinasesY 27632

Identifiers

PMID22521605
PMCPMC3598891
OpenAlexW2081851012

What OpenQuestion holds

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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.