Evidence map›Paper›PMID 20861353›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

NF-kappaB activation limits airway branching through inhibition of Sp1-mediated fibroblast growth factor-10 expression.

John T Benjamin, Billy J Carver, Erin J Plosa, Yasutoshi Yamamoto, J Davin Miller, Jin-Hua Liu, Riet van der Meer, Timothy S Blackwell, Lawrence S Prince

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
6.7field-weighted citation impact, top 3% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.

  1. Pooled it
  2. Review
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  14. Hyperoxia Injury in the Developing Lung Is Mediated by Mesenchymal Expression of Wnt5A.American journal of respiratory and critical care medicine · 2020
    Article
  15. Review
  16. Article
  17. Article
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  19. Article
  20. Consequences of early postnatal lipopolysaccharide exposure on developing lungs in mice.American journal of physiology. Lung cellular and molecular physiology · 2019
    Article

1 more citing papers are in PubMed but not listed here.

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

9 authors at 2 institutions in 2 countries.

John T BenjaminDivision of Neonatology, Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.
Billy J Carver
Erin J Plosa
Yasutoshi Yamamoto
J Davin Miller
Jin-Hua Liu
Riet van der Meer
Timothy S Blackwell
Lawrence S Prince
Vanderbilt University · USUniversity of Alabama at Birmingham · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI STACIE B DUSETZINA · 1995 to 2026
$172.8M
Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI ALVIN C POWERS · 2012 to 2026
$29.3M
TRANSGENIC MOUSE/ ES CELL SHARES RESOURCESP60DK020593 · NIDDK · VANDERBILT UNIVERSITY · PI POWERS, ALVIN C · 1986 to 2011
$28.1M
Shop Module CoreP30EY008126 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI David J. Calkins · 1989 to 2026
$19.6M
THREE-TIERED PREVENTION MODEL TO BETTER SERVE ALL STUDENP30HD015052 · NICHD · VANDERBILT UNIVERSITY · PI HARRELL, FRANK E. · 1985 to 2014
$18.6M
Vanderbilt Mouse Metabolic Physiology CenterU24DK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2001 to 2015
$14.9M
Vanderbilt Mouse Metabolic Phenotyping CenterU2CDK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2016 to 2021
$6.3M
FGF-10 Expression in a Fetal Mouse Lung Model of Bronchopulmonary DysplasiaR01HL086324 · NHLBI · VANDERBILT UNIVERSITY · PI PRINCE, LAWRENCE S · 2008 to 2017
$3.7M
Role of Fetal Lung Macrophages in Broncopulmonary DysplasiaR01HL097195 · NHLBI · VANDERBILT UNIVERSITY · PI BLACKWELL, TIMOTHY S., PRINCE, LAWRENCE S · 2009 to 2013
$2.6M
Role of NADPH Oxidase in Regulating InflammationR01AI079253 · NIAID · ROSWELL PARK CANCER INSTITUTE CORP · PI SEGAL, BRAHM H. · 2009 to 2013
$2.1M
NCI NIH HHS CA68485NCI NIH HHS P30 CA068485NEI NIH HHS EY08126NEI NIH HHS P30 EY008126NHLBI NIH HHS HL-086324NHLBI NIH HHS HL-097195NHLBI NIH HHS R01 HL086324NHLBI NIH HHS R01 HL097195NIAID NIH HHS AI-079253NIAID NIH HHS R01 AI079253NICHD NIH HHS HD15052NICHD NIH HHS P30 HD015052NIDDK NIH HHS DK20593NIDDK NIH HHS DK58404NIDDK NIH HHS DK59637NIDDK NIH HHS P30 DK020593NIDDK NIH HHS P30 DK058404NIDDK NIH HHS P60 DK020593NIDDK NIH HHS U24 DK059637
6 · The paper itself

Abstract

Bronchopulmonary dysplasia (BPD) is a frequent complication of preterm birth. This chronic lung disease results from arrested saccular airway development and is most common in infants exposed to inflammatory stimuli. In experimental models, inflammation inhibits expression of fibroblast growth factor-10 (FGF-10) and impairs epithelial-mesenchymal interactions during lung development; however, the mechanisms connecting inflammatory signaling with reduced growth factor expression are not yet understood. In this study we found that soluble inflammatory mediators present in tracheal fluid from preterm infants can prevent saccular airway branching. In addition, LPS treatment led to local production of mediators that inhibited airway branching and FGF-10 expression in LPS-resistant C.C3-Tlr4(Lpsd)/J fetal mouse lung explants. Both direct NF-κB activation and inflammatory cytokines (IL-1β and TNF-α) that activate NF-κB reduced FGF-10 expression, whereas chemokines that signal via other inflammatory pathways had no effect. Mutational analysis of the FGF-10 promoter failed to identify genetic elements required for direct NF-κB-mediated FGF-10 inhibition. Instead, NF-κB activation appeared to interfere with the normal stimulation of FGF-10 expression by Sp1. Chromatin immunoprecipitation and nuclear coimmunoprecipitation studies demonstrated that the RelA subunit of NF-κB and Sp1 physically interact at the FGF-10 promoter. These findings indicate that inflammatory signaling through NF-κB disrupts the normal expression of FGF-10 in fetal lung mesenchyme by interfering with the transcriptional machinery critical for lung morphogenesis.

Indexed as

AnimalsChorioamnionitisChromatin ImmunoprecipitationFemaleFibroblast Growth Factor 10Gene ExpressionGene Expression RegulationHumansImmunohistochemistryImmunoprecipitationInfant, NewbornLungMiceMice, Inbred BALB CNF-kappa BPregnancyFGF10 protein, humanFibroblast Growth Factor 10NF-kappa BProtein KinasesSp1 kinase

Identifiers

PMID20861353
PMCPMC4399641
OpenAlexW2168018540

What OpenQuestion holds

Textmetadata
LicenceTDM
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.