Evidence map›Paper›PMID 23558680›Full record

ArticleThe Journal of biological chemistry2013

Interactions between NF-κB and SP3 connect inflammatory signaling with reduced FGF-10 expression.

Billy J Carver, Erin J Plosa, Amanda M Stinnett, Timothy S Blackwell, Lawrence S Prince

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
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  20. The innate immune response in fetal lung mesenchymal cells targets VEGFR2 expression and activity.American journal of physiology. Lung cellular and molecular physiology · 2017
    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

5 authors at 2 institutions in 1 country.

Billy J CarverDepartment of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.
Erin J Plosa
Amanda M Stinnett
Timothy S Blackwell
Lawrence S Prince
Vanderbilt University · USUniversity of California, San Diego · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 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 OWEN P MCGUINNESS · 2012 to 2026
$29.3M
TRANSGENIC MOUSE/ ES CELL SHARES RESOURCESP60DK020593 · NIDDK · VANDERBILT UNIVERSITY · PI MCGUINNESS, OWEN P · 1986 to 2011
$28.1M
Shop Module CoreP30EY008126 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Kevin L Schey · 1989 to 2026
$19.6M
THREE-TIERED PREVENTION MODEL TO BETTER SERVE ALL STUDENP30HD015052 · NICHD · VANDERBILT UNIVERSITY · PI DYKENS, ELISABETH MAY · 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
Training Program in Stem Cell and Regenerative Developmental BiologyT32HD007502 · NICHD · VANDERBILT UNIVERSITY · PI WRIGHT, CHRISTOPHER V · 1997 to 2022
$5.4M
Conducting Child Health Care Research in Vulnerable PopulationsT32HD060554 · NICHD · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BARKIN, SHARI, WILLIAMS, DEREK J. · 2009 to 2019
$3.8M
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
NCI NIH HHS CA68485NCI NIH HHS P30 CA068485NEI NIH HHS EY08126NEI NIH HHS P30 EY008126NHLBI NIH HHS HL086324NHLBI NIH HHS HL086324-2S1NHLBI NIH HHS HL097195NHLBI NIH HHS R01 HL086324NHLBI NIH HHS R01 HL097195NICHD NIH HHS HD060554NICHD NIH HHS HD15052NICHD NIH HHS P30 HD015052NICHD NIH HHS T32 HD007502NICHD NIH HHS T32 HD060554NIDDK 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

Inflammation inhibits normal lung morphogenesis in preterm infants. Soluble inflammatory mediators present in the lungs of patients developing bronchopulmonary dysplasia disrupt expression of multiple genes critical for development. However, the mechanisms linking innate immune signaling and developmental programs are not clear. NF-κB activation inhibits expression of the critical morphogen FGF-10. Here, we show that interactions between the RELA subunit of NF-κB and SP3 suppress SP1-mediated FGF-10 expression. SP3 co-expression reduced SP1-mediated Fgf-10 promoter activity, suggesting antagonistic interactions between SP1 and SP3. Chromatin immunoprecipitation of LPS-treated primary mouse fetal lung mesenchymal cells detected increased interactions between SP3, RELA, and the Fgf-10 promoter. Expression of a constitutively active IκB kinase β mutant not only decreased Fgf-10 promoter activity but also increased RELA-SP3 nuclear interactions. Expression of a dominant-negative IκB, which blocks NF-κB nuclear translocation, prevented inhibition of FGF-10 by SP3. The inhibitory functions of SP3 required sequences located in the N-terminal region of the protein. These data suggested that inhibition of FGF-10 by inflammatory signaling involves the NF-κB-dependent interactions between RELA, SP3, and the Fgf-10 promoter. NF-κB activation may therefore lead to reduced gene expression by recruiting inhibitory factors to specific gene promoters following exposure to inflammatory stimuli.

Indexed as

Gene Expression RegulationResponse ElementsActive Transport, Cell NucleusAnimalsCell NucleusCHO CellsCricetinaeFetusFibroblast Growth Factor 10HumansImmunity, InnateInflammationLipopolysaccharidesLungMiceSp3 Transcription FactorFgf10 protein, mouseFibroblast Growth Factor 10LipopolysaccharidesRela protein, mouseSp3 protein, mouseSp3 Transcription FactorTranscription Factor RelABranching MorphogenesisCytokineFibroblast Growth Factor (FGF)Growth FactorsInflammationLungMorphogenesisNF-kappa B (NF-KB)Sp1

Identifiers

PMID23558680
PMCPMC3663551
OpenAlexW2095020383

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.