Evidence map›Paper›PMID 16357363›Full record

ArticleAmerican journal of respiratory cell and molecular biology2006

P53 mediates amosite asbestos-induced alveolar epithelial cell mitochondria-regulated apoptosis.

Vijayalakshmi Panduri, Sailesh Surapureddi, Saul Soberanes, Sigmund A Weitzman, Navdeep Chandel, David W Kamp

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 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.5field-weighted citation impact, top 5% 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, 73 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. p53: A Key Protein That Regulates Pulmonary Fibrosis.Oxidative medicine and cellular longevity · 2020
    Review
  7. Mitochondrial Dysfunction in Pulmonary Fibrosis.Annals of the American Thoracic Society · 2017
    Review
  8. Article
  9. Asbestos-induced pulmonary fibrosis is augmented in 8-oxoguanine DNA glycosylase knockout mice.American journal of respiratory cell and molecular biology · 2015
    Article
  10. Article
  11. Article
  12. Article
  13. Asbestos-Induced Gastrointestinal Cancer: An Update.Journal of gastrointestinal & digestive system · 2013
    Article
  14. Oxidative stress and pulmonary fibrosis.Biochimica et biophysica acta · 2013
    Review
  15. Molecular basis of asbestos-induced lung disease.Annual review of pathology · 2013
    Review
  16. Article
  17. Article
  18. Pulmonary endpoints (lung carcinomas and asbestosis) following inhalation exposure to asbestos.Journal of toxicology and environmental health. Part B, Critical reviews · 2011
    Review
  19. Role of mutagenicity in asbestos fiber-induced carcinogenicity and other diseases.Journal of toxicology and environmental health. Part B, Critical reviews · 2011
    Review
  20. 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.

Vijayalakshmi PanduriNorthwestern University Feinberg School of Medicine, Pulmonary and Critical Care Medicine, McGaw M-2300, 240 E. Huron St., Chicago, IL 60611-3010, USA.
Sailesh Surapureddi
Saul Soberanes
Sigmund A Weitzman
Navdeep Chandel
David W Kamp
Northwestern University · US

Funding

Role of LUBAC and Na K-ATPase in Acute Lung InjuryP01HL071643 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CHANDEL, NAVDEEP S · 2003 to 2019
$30.8M
MECHANISMS OF NFKB ACTIVATION IN HYPOXIA AND SEPSISR01GM060472 · NIGMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CHANDEL, NAVDEEP S · 2000 to 2008
$1.9M
NHLBI NIH HHS P01-HL-071643NIGMS NIH HHS GM-60472
6 · The paper itself

Abstract

Asbestos causes pulmonary toxicity in part by generating reactive oxygen species that cause DNA damage. We previously showed that the mitochondria-regulated (intrinsic) death pathway mediates alveolar epithelial cell (AEC) DNA damage and apoptosis. Because p53 regulates the DNA damage response in part by inducing intrinsic cell death, we determined whether p53-dependent transcriptional activity mediates asbestos-induced AEC mitochondrial dysfunction and apoptosis. We show that inhibitors of p53-dependent transcriptional activation (pifithrin and type 16-E6 protein) block asbestos-induced AEC mitochondrial membrane potential change (DeltaPsim), caspase 9 activation, and apoptosis. We demonstrate that asbestos activates p53 promoter activity, mRNA levels, protein expression, and Bax and p53 mitochondrial translocation. Further, pifithrin, E6, phytic acid, or rho(0)-A549 cells (cells incapable of mitochondrial reactive oxygen species production) block asbestos-induced p53 activation. Finally, we show that asbestos augments p53 expression in cells at the bronchoalveolar duct junctions of rat lungs and that phytic acid prevents this. These data suggest that p53-dependent transcription pathways mediate asbestos-induced AEC mitochondria-regulated apoptosis. This suggests an important interactive effect between p53 and the mitochondria in the pathogenesis of asbestos-induced pulmonary toxicity that may have broader implications for our understanding of pulmonary fibrosis and lung cancer.

Indexed as

ApoptosisAnimalsAsbestos, AmositeAsbestosisbcl-2-Associated X ProteinBenzothiazolesCaspase 9CaspasesCell LineEnzyme ActivationEpithelial CellsFree Radical ScavengersHumansIron Chelating AgentsLungMembrane PotentialsAsbestos, Amositebcl-2-Associated X ProteinBenzothiazolesCASP9 protein, humanCasp9 protein, ratCaspase 9CaspasesE6 protein, Human papillomavirus type 16Free Radical ScavengersIron Chelating AgentsOncogene Proteins, ViralPhytic AcidpifithrinReactive Oxygen SpeciesRepressor ProteinsThiazolesTolueneTumor Suppressor Protein p53

Identifiers

PMID16357363
PMCPMC2644206
OpenAlexW2107182759

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.