Evidence map›Paper›PMID 20711931›Full record

ArticleJournal of toxicology and environmental health. Part A2010

Effects of cigarette smoke on the activation of oxidative stress-related transcription factors in female A/J mouse lung.

Job C Tharappel, Jill Cholewa, Parvaneh Espandiari, Brett T Spear, C Gary Gairola, Howard P Glauert

Abstract read
In one paragraph

Article in Journal of toxicology and environmental health. Part A, 2010. 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
1.1field-weighted citation impact, top 24% 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, 26 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. The Association Between Smoking and Gut Microbiome in Bangladesh.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2020
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Malignancy risk models for oral lesions.Medicina oral, patologia oral y cirugia bucal · 2013
    Article
  12. Article
  13. Article
  14. Article
  15. 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 5 institutions in 3 countries.

Job C TharappelGraduate Center for Nutritional Sciences, University of Kentucky, Lexington, KY 40506-0054, USA.
Jill Cholewa
Parvaneh Espandiari
Brett T Spear
C Gary Gairola
Howard P Glauert
University of Kentucky · USLaboratory of Molecular Genetics · PLNutrition Sciences (Belgium) · BESociety of Environmental Toxicology and Chemistry · USThe Graduate Center, CUNY · US

Funding

TRAINING PROGRAM IN OXIDATIVE STRESS AND NUTRITIONT32DK007778 · NIDDK · UNIVERSITY OF KENTUCKY · PI WEBB, NANCY R · 2000 to 2019
$2.5M
NIDDK NIH HHS DK07778NIDDK NIH HHS T32 DK007778
6 · The paper itself

Abstract

Cigarette smoke contains a high concentration of free radicals and induces oxidative stress in the lung and other tissues. Several transcription factors are known to be activated by oxidative stress, including nuclear factor-kappaB (NF-kappaB), activator protein-1 (AP-1), and hypoxia-inducible factor (HIF). Studies were therefore undertaken to examine whether cigarette smoke could activate these transcription factors, as well as other transcription factors that may be important in lung carcinogenesis. Female A/J mice were exposed to cigarette smoke for 2, 5, 10, 15, 20, 42, or 56 d (6 hr/d, 5 d/wk). Cigarette smoke did not increase NF-kappaB activation at any of these times, but NF-kappaB DNA binding activity was lower after 15 d and 56 d of smoke exposure. The DNA binding activity of AP-1 was lower after 10 d and 56 d but was not changed after 42 d of smoke exposure. The DNA binding activity of HIF was quantitatively increased after 42 d of smoke exposure but decreased after 56 d. Whether the activation of other transcription factors in the lung could be altered after exposure to cigarette smoke was subsequently examined. The DNA binding activities of FoxF2, myc-CF1, RORE, and p53 were examined after 10 d of smoke exposure. The DNA binding activities of FoxF2 and p53 were quantitatively increased, but those of myc-CF1 and RORE were unaffected. These studies show that cigarette smoke exposure leads to quantitative increases in DNA binding activities of FoxF2 and p53, while the activations of NF-kappaB, AP-1, and HIF are largely unaffected or reduced.

Indexed as

AnimalsBlotting, WesternDNAElectrophoretic Mobility Shift AssayFemaleGene Expression RegulationHypoxia-Inducible Factor 1LungMiceMice, Inbred ANF-kappa BOxidative StressTime FactorsTobacco Smoke PollutionTranscription Factor AP-1Transcription FactorsDNAHypoxia-Inducible Factor 1NF-kappa BTobacco Smoke PollutionTranscription Factor AP-1Transcription Factors

Identifiers

PMID20711931
PMCPMC2924761
OpenAlexW2093513682

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.