Evidence map›Paper›PMID 26545977›Full record

ArticleBMC pulmonary medicine2015

Plakoglobin expression in fibroblasts and its role in idiopathic pulmonary fibrosis.

Stephanie A Matthes, Thomas J LaRouere, Jeffrey C Horowitz, Eric S White

Open access · goldAbstract read
In one paragraph

Article in BMC pulmonary medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.5field-weighted citation impact, top 30% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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

4 authors at 1 institution in 1 country.

Stephanie A MatthesDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, 48109-5642, USA. saboeck@med.umich.edu.
Thomas J LaRouereDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, 48109-5642, USA. tlarouere@gmail.com.
Jeffrey C HorowitzDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, 48109-5642, USA. jchorow@med.umich.edu.
Eric S WhiteDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, 48109-5642, USA. docew@med.umich.edu.
University of Michigan–Ann Arbor · US

Funding

PULMONARY CELLULAR AND MOLECULAR BIOLOGY TRAININGT32HL007749 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Robert Pickett Dickson · 1993 to 2026
$19.9M
Matrix and Bioreactors for Human Lung RegenerationU01HL111016 · NHLBI · YALE UNIVERSITY · PI NIKLASON, LAURA E, WHITE, ERIC S · 2012 to 2016
$3.2M
Mesenchymal Cell Fate Determination by Extracellular Matrix StiffnessR01HL105489 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HOROWITZ, JEFFREY C · 2011 to 2015
$1.9M
Matrix biomarkers and compartmentalization in IPFR01HL109118 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WHITE, ERIC S · 2012 to 2015
$1.8M
NHLBI NIH HHS HL105489NHLBI NIH HHS R01 HL105489NHLBI NIH HHS R01 HL109118NHLBI NIH HHS T32 HL007749NHLBI NIH HHS T32 HL07749NHLBI NIH HHS U01 HL111016
6 · The paper itself

Abstract

backgroundIdiopathic pulmonary fibrosis (IPF) is an interstitial fibrotic lung disease of unknown origin and without effective therapy characterized by deposition of extracellular matrix by activated fibroblasts in the lung. Fibroblast activation in IPF is associated with Wnt/β-catenin signaling, but little is known about the role of the β-catenin-homologous desmosomal protein, plakoglobin (PG), in IPF. The objective of this study was to assess the functional role of PG in human lung fibroblasts in IPF.

methodsHuman lung fibroblasts from normal or IPF patients were transfected with siRNA targeting PG and used to assess cellular adhesion to a fibronectin substrate, apoptosis and proliferation. Statistical analysis was performed using Student's t-test with Mann-Whitney post-hoc analyses and results were considered significant when p < 0.05.

resultsWe found that IPF lung fibroblasts expressed less PG protein than control fibroblasts, but that characteristic fibroblast phenotypes (adhesion, proliferation, and apoptosis) were not controlled by PG expression. Consistent with this, normal fibroblasts in which PG was silenced displayed no change in functional phenotype.

conclusionsWe conclude that diminished PG levels in IPF lung fibroblasts do not directly affect certain phenotypic behaviors. Further study is needed to identify the functional consequences of decreased PG in these cells.

Indexed as

ApoptosisBlotting, WesternCase-Control StudiesCell AdhesionCell ProliferationCells, CulturedDesmoplakinsFibroblastsFibronectinsgamma CateninGene Knockdown TechniquesHumansIdiopathic Pulmonary FibrosisReal-Time Polymerase Chain ReactionRNA, MessengerDesmoplakinsFibronectinsgamma CateninJUP protein, humanRNA, Messenger

Identifiers

PMID26545977
PMCPMC4636798
OpenAlexW2157245642

What OpenQuestion holds

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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.