Evidence map›Paper›PMID 15993334›Full record

ArticleFree radical biology & medicine2005

HNE increases HO-1 through activation of the ERK pathway in pulmonary epithelial cells.

Karen E Iles, Dale A Dickinson, Amanda F Wigley, Nathan E Welty, Volker Blank, Henry Jay Forman

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 103 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Effects of Inhaled Tobacco Smoke on the Pulmonary Tumor Microenvironment.Advances in experimental medicine and biology · 2020
    Review
  7. Article
  8. Review
  9. Article
  10. 4-hydroxynonenal-mediated signaling and aging.Free radical biology & medicine · 2017
    Review
  11. Review
  12. Article
  13. Review
  14. Modeling head and neck cancer stem cell-mediated tumorigenesis.Cellular and molecular life sciences : CMLS · 2016
    Review
  15. Article
  16. Article
  17. Effect of ERK1/2 signaling pathway in electro-acupuncture mediated up-regulation of heme oxygenase-1 in lungs of rabbits with endotoxic shock.Medical science monitor : international medical journal of experimental and clinical research · 2014
    Article
  18. Article
  19. Review
  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

6 authors at 3 institutions in 2 countries.

Karen E IlesDepartment of Environmental Health Sciences, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Dale A Dickinson
Amanda F Wigley
Nathan E Welty
Volker Blank
Henry Jay Forman
University of Alabama at Birmingham · USJewish General Hospital · CAUniversity of California, Merced · US

Funding

REGULATION OF GLUTATHIONE SYNTHESIS IN OXIDATIVE STRESSR01ES005511 · NIEHS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI FORMAN, HENRY JAY · 1991 to 2010
$2.9M
Hydroxynonenal induces glutathione synthesis through JNKR56ES005511 · NIEHS · UNIVERSITY OF CALIFORNIA, MERCED · PI FORMAN, HENRY JAY · 2006 to 2006
$75k
NIEHS NIH HHS ES05511NIEHS NIH HHS R01 ES005511NIEHS NIH HHS R56 ES005511
6 · The paper itself

Abstract

Heme oxygenase-1 (HO-1) is a key cytoprotective enzyme and an established marker of oxidative stress. Increased HO-1 expression has been found in the resident macrophages in the alveolar spaces of smokers. The lipid peroxidation product 4-hydroxynonenal (HNE) is also increased in the bronchial and alveolar epithelium in response to cigarette smoke. This suggests a link between a chronic environmental stress, HNE formation, and HO-1 induction. HNE is both an agent of oxidative stress in vivo and a potent cell signaling molecule. We hypothesize that HNE acts as an endogenously produced pulmonary signaling molecule that elicits an adaptive response culminating in the induction of HO-1. Here we demonstrate that HNE increases HO-1 mRNA, protein, and activity in pulmonary epithelial cells and identify ERK as a key pathway involved. Treatment with HNE increased ERK phosphorylation, c-Fos protein, JNK phosphorylation, c-Jun phosphorylation, and AP-1 binding. Whereas inhibiting the ERK pathway with the MEK inhibitor PD98059 significantly decreased HNE-mediated ERK phosphorylation, c-Fos protein induction, AP-1 binding, and HO-1 protein induction, inhibition of the ERK pathway had no effect on HNE-induced HO-1 mRNA. This suggests that ERK is involved in the increase in HO-1 through regulation of translation rather than transcription.

Indexed as

AldehydesAnimalsAnthracenesBlotting, WesternCell LineCysteine Proteinase InhibitorsElectrophoretic Mobility Shift AssayEnzyme ActivationEpitheliumExtracellular Signal-Regulated MAP KinasesHeme Oxygenase-1Heme Oxygenase (Decyclizing)LungOxidative StressProtein BiosynthesisRats4-hydroxy-2-nonenalAldehydesAnthracenesCysteine Proteinase InhibitorsExtracellular Signal-Regulated MAP KinasesHeme Oxygenase-1Heme Oxygenase (Decyclizing)pyrazolanthroneRNA, Messenger

Identifiers

PMID15993334
PMCPMC2798573
OpenAlexW1973019265

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.