Evidence map›Paper›PMID 22773697›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012

Mitochondrial DNA-depleted A549 cells are resistant to bleomycin.

Sukhdev S Brar, Joel N Meyer, Carl D Bortner, Bennett Van Houten, William J Martin

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Review
  3. Oncology letters · 2024
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  9. Cybrid Models of Pathological Cell Processes in Different Diseases.Oxidative medicine and cellular longevity · 2018
    Review
  10. Article
  11. SIRT3 deficiency promotes lung fibrosis by augmenting alveolar epithelial cell mitochondrial DNA damage and apoptosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  12. Article
  13. SIRT3 blocks myofibroblast differentiation and pulmonary fibrosis by preventing mitochondrial DNA damage.American journal of physiology. Lung cellular and molecular physiology · 2017
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Animal models of systemic sclerosis: their utility and limitations.Open access rheumatology : research and reviews · 2014
    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

5 authors at 4 institutions in 1 country.

Sukhdev S BrarLaboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA.
Joel N Meyer
Carl D Bortner
Bennett Van Houten
William J Martin
National Institutes of Health · USDuke University · USNational Institute of Environmental Health Sciences · USUniversity of Pittsburgh · US

Funding

Flow CytometryZICES102486 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BORTNER, CARL · 2009 to 2025
$24.0M
Intramural NIH HHS
6 · The paper itself

Abstract

Alveolar epithelial cells are considered to be the primary target of bleomycin-induced lung injury, leading to interstitial fibrosis. The molecular mechanisms by which bleomycin causes this damage are poorly understood but are suspected to involve generation of reactive oxygen species and DNA damage. We studied the effect of bleomycin on mitochondrial DNA (mtDNA) and nuclear DNA (nDNA) in human alveolar epithelial A549 cells. Bleomycin caused an increase in reactive oxygen species production, DNA damage, and apoptosis in A549 cells; however, bleomycin induced more mtDNA than nDNA damage. DNA damage was associated with activation of caspase-3, cleavage of poly(ADP-ribose) polymerase, and cleavage and activation of protein kinase D1 (PKD1), a newly identified mitochondrial oxidative stress sensor. These effects appear to be mtDNA-dependent, because no caspase-3 or PKD1 activation was observed in mtDNA-depleted (ρ(0)) A549 cells. Survival rate after bleomycin treatment was higher for A549 ρ(0) than A549 cells. These results suggest that A549 ρ(0) cells are more resistant to bleomycin toxicity than are parent A549 cells, likely in part due to the depletion of mtDNA and impairment of mitochondria-dependent apoptotic pathways.

Indexed as

Drug Resistance, NeoplasmAdenosine TriphosphateAntibiotics, AntineoplasticApoptosisbcl-2-Associated X ProteinBleomycinCaspase 3Cell Line, TumorCell NucleusDNA DamageDNA, MitochondrialEnzyme ActivationGene ExpressionHumansMembrane Potential, MitochondrialMitochondriaAdenosine TriphosphateAntibiotics, AntineoplasticBAX protein, humanbcl-2-Associated X ProteinBleomycinCASP3 protein, humanCaspase 3DNA, MitochondrialReactive Oxygen SpeciesTRPP Cation Channels

Identifiers

PMID22773697
PMCPMC3468425
OpenAlexW2147325553

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.