Evidence map›Paper›PMID 23885834›Full record

ArticleAmerican journal of respiratory cell and molecular biology2013

Asbestos-induced alveolar epithelial cell apoptosis. The role of endoplasmic reticulum stress response.

David W Kamp, Gang Liu, Paul Cheresh, Seok-Jo Kim, Amanda Mueller, Anna P Lam, Humberto Trejo, David Williams, Sandhya Tulasiram, Margaret Baker and 3 more

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

36 citing papers in PubMed, 63 citations in OpenAlex.

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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

13 authors at 1 institution in 2 countries.

David W Kamp1 Department of Medicine, Division of Pulmonary & Critical Care Medicine, Jesse Brown Veterans Affairs Medical Center and Northwestern University Feinberg School of Medicine, Chicago, Illinois; and.
Gang Liu
Paul Cheresh
Seok-Jo Kim
Amanda Mueller
Anna P Lam
Humberto Trejo
David Williams
Sandhya Tulasiram
Margaret Baker
Karen Ridge
Navdeep S Chandel
Rohinee Beri
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
Mitigation of asbestos induced alveolar epithelial cell injuryR01ES020357 · NIEHS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI KAMP, DAVID W · 2012 to 2016
$1.6M
Recruitment of New Faculty to Enhance Research in Lung BiologyP30HL101292 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SZNAJDER, JACOB I · 2009 to 2010
$887k
BLRD VA I01 BX000786NHLBI NIH HHS P01 HL071643NHLBI NIH HHS P01HL071643NHLBI NIH HHS P30 HL101292NIEHS NIH HHS R01 ES020357NIEHS NIH HHS R01ES020357
6 · The paper itself

Abstract

Asbestos exposure results in pulmonary fibrosis (asbestosis) and malignancies (bronchogenic lung cancer and mesothelioma) by mechanisms that are not fully understood. Alveolar epithelial cell (AEC) apoptosis is important in the development of pulmonary fibrosis after exposure to an array of toxins, including asbestos. An endoplasmic reticulum (ER) stress response and mitochondria-regulated (intrinsic) apoptosis occur in AECs of patients with idiopathic pulmonary fibrosis, a disease with similarities to asbestosis. Asbestos induces AEC intrinsic apoptosis, but the role of the ER is unclear. The objective of this study was to determine whether asbestos causes an AEC ER stress response that promotes apoptosis. Using human A549 and rat primary isolated alveolar type II cells, amosite asbestos fibers increased AEC mRNA and protein expression of ER stress proteins involved in the unfolded protein response, such as inositol-requiring kinase (IRE) 1 and X-box-binding protein-1, as well as ER Ca²(2+) release ,as assessed by a FURA-2 assay. Eukarion-134, a superoxide dismutase/catalase mimetic, as well as overexpression of Bcl-XL in A549 cells each attenuate asbestos-induced AEC ER stress (IRE-1 and X-box-binding protein-1 protein expression; ER Ca²(2+) release) and apoptosis. Thapsigargin, a known ER stress inducer, augments AEC apoptosis, and eukarion-134 or Bcl-XL overexpression are protective. Finally, 4-phenylbutyric acid, a chemical chaperone that attenuates ER stress, blocks asbestos- and thapsigargin-induced AEC IRE-1 protein expression, but does not reduce ER Ca²(2+) release or apoptosis. These results show that asbestos triggers an AEC ER stress response and subsequent intrinsic apoptosis that is mediated in part by ER Ca²(2+) release.

Indexed as

Alveolar Epithelial CellsAnimalsAntioxidantsApoptosisAsbestos, Amositebcl-X ProteinCalcium SignalingCell LineCells, CulturedDNA-Binding ProteinsEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressEndoribonucleasesHeat-Shock ProteinsHumansMembrane Proteins4-phenylbutyric acidAntioxidantsAsbestos, AmositeBCL2L1 protein, humanbcl-X ProteinDDIT3 protein, humanDNA-Binding ProteinsEndoplasmic Reticulum Chaperone BiPEndoribonucleasesERN2 protein, humanEUK-134Heat-Shock ProteinsMembrane ProteinsOrganometallic CompoundsPhenylbutyratesProtein Serine-Threonine KinasesRegulatory Factor X Transcription FactorsRNA, MessengerSalicylatesThapsigarginTranscription Factor CHOPTranscription Factors

Identifiers

PMID23885834
PMCPMC3931115
OpenAlexW2113186524

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.