Evidence map›Paper›PMID 19730131›Full record

ArticleJournal of investigative medicine : the official publication of the American Federation for Clinical Research2009

Delineation of a gene network underlying the pulmonary response to oxidative stress in asthma.

Robert J Freishtat, Angela S Benton, Alan M Watson, Zuyi Wang, Mary C Rose, Eric P Hoffman

Abstract read
In one paragraph

Article in Journal of investigative medicine : the official publication of the American Federation for Clinical Research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

12 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Loss-of-function thrombospondin-1 mutations in familial pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2012
    Article
  9. Article
  10. Asthmatic airway epithelium is intrinsically inflammatory and mitotically dyssynchronous.American journal of respiratory cell and molecular biology · 2011
    Article
  11. Article
  12. 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.

Robert J FreishtatDivision of Emergency Medicine, Children's National Medical Center, The George Washington University, 111 Michigan Avenue NW, Washington, DC 20010, USA. rfreishtat@cnmcresearch.org
Angela S Benton
Alan M Watson
Zuyi Wang
Mary C Rose
Eric P Hoffman

Funding

Genetics and Genomic Approaches to Lung Diseases and Disorders in Washington, DCK12HL090020 · NHLBI · CHILDREN'S RESEARCH INSTITUTE · PI HOFFMAN, ERIC P. · 2007 to 2012
$2.0M
MENTORED PATIENT-ORIENTED RESEARCH CAREEER DEVELOPMENT AWARDK23RR020069 · NCRR · CHILDREN'S RESEARCH INSTITUTE · PI FREISHTAT, ROBERT J · 2005 to 2009
$623k
NCRR NIH HHS K23 RR020069NCRR NIH HHS K23-RR-020069NHLBI NIH HHS K12 HL090020NHLBI NIH HHS L40 HL074778
6 · The paper itself

Abstract

Cigarette smoke exposure induces a respiratory epithelial response that is mediated in part by oxidative stress. The contribution of oxidative stress to cigarette smoke-induced responses in asthmatic respiratory epithelium is not well understood. We sought to increase this understanding by employing data integration and systems biology approaches to publicly available microarray data deposited over the last several years. In this study, we analyzed 14 publicly available asthma- or tobacco-relevant data series and found 4 (2 mice and 2 human) that fulfilled adequate signal/noise thresholds using unsupervised clustering and F test statistics. Using significance filters and a 4-way Venn diagram approach, we identified 26 overlapping genes in the epithelial transcriptional stress response to cigarette smoke and asthma. This test set corresponded to a 26-member gene/protein network containing 18 members that were highly regulated in a fifth data series of direct lung oxidative stress. Of those network members, 2 stood out (ie, tissue inhibitor of metalloproteinase 1 and thrombospondin 1) owing to central location within the network and marked up-regulation sustained at later times in response to oxidative stress. These analyses identified key relationships and primary hypothetical targets for future studies of cigarette smoke-induced oxidative stress in asthma.

Indexed as

Gene Regulatory NetworksAnimalsAsthmaCell LineDatabases, GeneticGene Expression ProfilingGenome-Wide Association StudyHumansLungMiceMice, Inbred StrainsOligonucleotide Array Sequence AnalysisOxidative StressPhosgeneSmokingSystems BiologyPhosgeneThrombospondinsTissue Inhibitor of Metalloproteinase-1

Identifiers

PMID19730131
PMCPMC3328512

What OpenQuestion holds

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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.