Evidence map›Paper›PMID 24647608›Full record

ArticlePloS one2014

Transcriptome analysis reveals differential splicing events in IPF lung tissue.

Tracy Nance, Kevin S Smith, Vanessa Anaya, Rhea Richardson, Lawrence Ho, Mauro Pala, Sara Mostafavi, Alexis Battle, Carol Feghali-Bostwick, Glenn Rosen and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
4.8field-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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.

  1. Pooled it
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  17. Inhibitors of the Sialidase NEU3 as Potential Therapeutics for Fibrosis.International journal of molecular sciences · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Tracy NanceDepartment of Pathology, Stanford University, Stanford, California, United States of America.
Kevin S SmithDepartment of Pathology, Stanford University, Stanford, California, United States of America.
Vanessa AnayaDepartment of Pathology, Stanford University, Stanford, California, United States of America.
Rhea RichardsonDepartment of Pathology, Stanford University, Stanford, California, United States of America.
Lawrence HoDivision of Pulmonary and Critical Care Medicine, University of Washington, Seattle, Washington, United States of America.
Mauro PalaDepartment of Pathology, Stanford University, Stanford, California, United States of America.
Sara MostafaviDepartment of Computer Science, Stanford University, Stanford, California, United States of America.
Alexis BattleDepartment of Computer Science, Stanford University, Stanford, California, United States of America.
Carol Feghali-BostwickDivision of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States of America.
Glenn RosenDepartment of Medicine, Division of Pulmonary and Critical Care Medicine, Stanford University, Stanford, California, United States of America.
Stephen B MontgomeryDepartment of Pathology, Stanford University, Stanford, California, United States of America.
Stanford University · USUniversity of Pittsburgh · USUniversity of Washington · US

Funding

INSTITUTIONAL TRAINING GRANT IN GENOME SCIENCET32HG000044 · NHGRI · STANFORD UNIVERSITY · PI MICHAEL P. SNYDER · 1995 to 2026
$32.2M
NHGRI NIH HHS T32 HG000044
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a complex disease in which a multitude of proteins and networks are disrupted. Interrogation of the transcriptome through RNA sequencing (RNA-Seq) enables the determination of genes whose differential expression is most significant in IPF, as well as the detection of alternative splicing events which are not easily observed with traditional microarray experiments. We sequenced messenger RNA from 8 IPF lung samples and 7 healthy controls on an Illumina HiSeq 2000, and found evidence for substantial differential gene expression and differential splicing. 873 genes were differentially expressed in IPF (FDR<5%), and 440 unique genes had significant differential splicing events in at least one exonic region (FDR<5%). We used qPCR to validate the differential exon usage in the second and third most significant exonic regions, in the genes COL6A3 (RNA-Seq adjusted pval = 7.18e-10) and POSTN (RNA-Seq adjusted pval = 2.06e-09), which encode the extracellular matrix proteins collagen alpha-3(VI) and periostin. The increased gene-level expression of periostin has been associated with IPF and its clinical progression, but its differential splicing has not been studied in the context of this disease. Our results suggest that alternative splicing of these and other genes may be involved in the pathogenesis of IPF. We have developed an interactive web application which allows users to explore the results of our RNA-Seq experiment, as well as those of two previously published microarray experiments, and we hope that this will serve as a resource for future investigations of gene regulation in IPF.

Indexed as

Gene Expression ProfilingAlternative SplicingCell Adhesion MoleculesCluster AnalysisCollagen Type VIDemographyDown-RegulationExonsGene Regulatory NetworksGenome-Wide Association StudyHumansIdiopathic Pulmonary FibrosisLungPolymerase Chain ReactionPolymorphism, Single NucleotideReproducibility of ResultsCell Adhesion MoleculesCollagen Type VIPOSTN protein, human

Identifiers

PMID24647608
PMCPMC3960165
OpenAlexW2168864202

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.