Evidence map›Paper›PMID 16601242›Full record

ArticleAmerican journal of respiratory cell and molecular biology2006

Cigarette smoke-induced Egr-1 upregulates proinflammatory cytokines in pulmonary epithelial cells.

Paul R Reynolds, Manuel G Cosio, John R Hoidal

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 106 citations in OpenAlex.

  1. Article
  2. Review
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  7. Article
  8. Role of early growth response 1 in inflammation-associated lung diseases.American journal of physiology. Lung cellular and molecular physiology · 2023
    Review
  9. Verproside, the Most Active Ingredient in YPL-001 Isolated fromInternational journal of molecular sciences · 2023
    Article
  10. Article
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  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. TLRs in pulmonary diseases.Life sciences · 2019
    Review
  19. Article
  20. 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

3 authors at 1 institution in 2 countries.

Paul R ReynoldsDepartment of Internal Medicine, Pulmonary Division, University of Utah Health Sciences Center, Salt Lake City, Utah, USA.
Manuel G Cosio
John R Hoidal
University of Utah · US

Funding

Nicotine Abuse /Smoking-Related Disease SusceptibilityP01HL072903 · NHLBI · UNIVERSITY OF UTAH · PI METHERALL, JAMES E · 2002 to 2006
$11.1M
NHLBI NIH HHS HL07636NHLBI NIH HHS HL72903
6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death worldwide and is a progressive and irreversible disorder. Cigarette smoking is associated with 80-90% of COPD cases; however, the genes involved in COPD-associated emphysema and chronic inflammation are poorly understood. It was recently demonstrated that early growth response gene 1 (Egr-1) is significantly upregulated in the lungs of smokers with COPD (Ning W and coworkers, Proc Natl Acad Sci 2004;101:14895-14900). We hypothesized that Egr-1 is activated in pulmonary epithelial cells during exposure to cigarette smoke extract (CSE). Using immunohistochemistry, we demonstrated that pulmonary adenocarcinoma cells (A-549) and primary epithelial cells lacking basal Egr-1 markedly induce Egr-1 expression after CSE exposure. To evaluate Egr-1-specific effects, we used antisense (alphaS) oligodeoxynucleotides (ODN) to knock down Egr-1 expression. Incorporation of Egr-1 alphaS ODN significantly decreased CSE-induced Egr-1 mRNA and protein, while sense ODN had no effect. Via Egr-1-mediated mechanisms, IL-1beta and TNF-alpha were significantly upregulated in pulmonary epithelial cells exposed to CSE or transfected with Egr-1. To investigate the relationship between Egr-1 induction by smoking and susceptibility to emphysema, we determined Egr-1 expression in strains of mice with different susceptibilities for the development of smoking-induced emphysema. Egr-1 was markedly increased in the lungs of emphysema-susceptible AKR/J mice chronically exposed to cigarette smoke, but only minimally increased in resistant NZWLac/J mice. In conclusion, Egr-1 is induced by cigarette smoke and functions in proinflammatory mechanisms that likely contribute to the development of COPD in the lungs of smokers.

Indexed as

AnimalsCytokinesDNA, AntisenseEarly Growth Response Protein 1Epithelial CellsHumansLungMicePulmonary EmphysemaSmokingTumor Cells, CulturedUp-RegulationCytokinesDNA, AntisenseEarly Growth Response Protein 1EGR1 protein, human

Identifiers

PMID16601242
PMCPMC2643284
OpenAlexW2019737644

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.