Evidence map›Paper›PMID 24970700›Full record

ArticleJournal of innate immunity2014

The transcription factor nuclear factor of activated T cells c3 modulates the function of macrophages in sepsis.

Ravi Ranjan, Jing Deng, Sangwoon Chung, Yong Gyu Lee, Gye Young Park, Lei Xiao, Myungsoo Joo, John William Christman, Manjula Karpurapu

Open access · bronzeAbstract read
In one paragraph

Article in Journal of innate immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

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  20. The Origin of a Paradigm.Journal of innate immunity · 2016
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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 3 institutions in 2 countries.

Ravi RanjanDepartment of Medicine and Section of Pulmonary, Critical Care, Sleep and Allergy, Department of Medicine, University of Illinois, Chicago, Ill., USA.
Jing Deng
Sangwoon Chung
Yong Gyu Lee
Gye Young Park
Lei Xiao
Myungsoo Joo
John William Christman
Manjula Karpurapu
The Ohio State University · USPusan National University · KRUniversity of Illinois Chicago · US

Funding

Macrophage Gene Expression in Acute Lung InflammationR01HL075557 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI CHRISTMAN, JOHN W · 2004 to 2016
$4.8M
Pulmonary and Critical Care Post-Doctoral Research Training ProgramT32HL082547 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI FINN, PATRICIA W · 2007 to 2017
$2.7M
NADPH OXIDASE REGULATION OF THE MACROPHAGE INFLAMMATORY PHENOTYPE IN SEPSISR01HL103643 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI CHRISTMAN, JOHN W · 2010 to 2013
$1.5M
Regulation of Neutrophilic Lung InflammationI01BX000108 · VA · JESSE BROWN VA MEDICAL CENTER · PI CHRISTMAN, JOHN W · 2009 to 2013
–
BLRD VA I01 BX000108NHLBI NIH HHS HL068610NHLBI NIH HHS R01 HL075557NHLBI NIH HHS R01 HL103643NHLBI NIH HHS T32 HL082547NHLBI NIH HHS T32HL082547
6 · The paper itself

Abstract

The role of the transcription factor nuclear factor of activated T cells (NFAT) was initially identified in T and B cell gene expression, but its role in regulating gene expression in macrophages during sepsis is not known. Our data show that NFATc3 regulates expression of inducible nitric oxide synthase (iNOS) in macrophages stimulated with lipopolysaccharide. Selective inhibition of NFAT by cyclosporine A and a competitive peptide inhibitor 11R-VIVIT inhibited endotoxin-induced expression of iNOS and nitric oxide (NO) release. Macrophages from NFATc3 knockout (KO) mice show reduced iNOS expression and NO release and attenuated bactericidal activity. Gel shift and chromatin immunoprecipitation assays show that endotoxin challenge increases NFATc3 binding to the iNOS promoter, resulting in transcriptional activation of iNOS. The binding of NFATc3 to the iNOS promoter is abolished by NFAT inhibitors. NFATc3 KO mice subjected to sepsis show that NFATc3 is necessary for bacterial clearance in mouse lungs during sepsis. Our study demonstrates for the first time that NFATc3 is necessary for macrophage iNOS expression during sepsis, which is essential for containment of bacterial infections.

Indexed as

AnimalsCell Line, TransformedCyclosporineEndotoxinsImmunosuppressive AgentsMacrophagesMiceMice, KnockoutNFATC Transcription FactorsNitric Oxide Synthase Type IIRatsResponse ElementsSepsisCyclosporineEndotoxinsImmunosuppressive AgentsNfatc3 protein, mouseNFATC Transcription FactorsNitric Oxide Synthase Type IINos2 protein, mouse

Identifiers

PMID24970700
PMCPMC4201910
OpenAlexW1972528075

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.