Evidence map›Paper›PMID 20615570›Full record

ArticleJournal of hepatology2010

Early growth response-1 attenuates liver injury and promotes hepatoprotection after carbon tetrachloride exposure in mice.

Michele T Pritchard, Jessica I Cohen, Sanjoy Roychowdhury, Brian T Pratt, Laura E Nagy

Open access · greenAbstract read
In one paragraph

Article in Journal of hepatology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

36 citing papers in PubMed, 52 citations in OpenAlex.

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  9. Ameliorative Effect of Graviola (Animals : an open access journal from MDPI · 2020
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  10. Anthocyanins Protect Hepatocytes against CClAntioxidants (Basel, Switzerland) · 2019
    Article
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  15. Thyroid hormones inhibit TGF-β signaling and attenuate fibrotic responses.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
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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

5 authors at 2 institutions in 1 country.

Michele T PritchardDepartment of Pathobiology, Cleveland Clinic, Cleveland, OH 44195, USA. pritchm@ccf.org
Jessica I Cohen
Sanjoy Roychowdhury
Brian T Pratt
Laura E Nagy
Cleveland Clinic · USCase Western Reserve University · US

Funding

Egr1: A candidate molecular target for treating ALD.R01AA013868 · NIAAA · CLEVELAND CLINIC LERNER COM-CWRU · PI NAGY, LAURA E. · 2004 to 2008
$1.5M
Liver fibrosis and ethanol: role of the transcription factor, Egr-1R00AA017918 · NIAAA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI PRITCHARD, MICHELE T · 2011 to 2013
$721k
Liver fibrosis and ethanol: role of the transcription factor, Egr-1K99AA017918 · NIAAA · CLEVELAND CLINIC LERNER COM-CWRU · PI PRITCHARD, MICHELE T · 2009 to 2010
$217k
Egr-1 and EtOH-induced hepatic leukocyte recruitmentF32AA015833 · NIAAA · CLEVELAND CLINIC LERNER COM-CWRU · PI PRITCHARD, MICHELE T · 2005 to 2006
$99k
NIAAA NIH HHS AA0138868NIAAA NIH HHS AA015833NIAAA NIH HHS AA017918NIAAA NIH HHS F32 AA015833NIAAA NIH HHS K99 AA017918NIAAA NIH HHS R00 AA017918NIAAA NIH HHS R01 AA013868
6 · The paper itself

Abstract

BACKGROUND &

aimsInflammatory gene expression plays a pathological role in acute and chronic hepatic inflammation, yet, inflammation also promotes liver repair by inducing protective mechanisms to limit collateral tissue damage by priming hepatocytes for proliferation. Early growth response (Egr)-1, a transcription factor that regulates inflammatory gene expression, plays a pathological role in many animal models of acute and chronic inflammatory disease. Here, we tested the hypothesis that Egr-1 is beneficial after toxic liver injury.

methodsAcute liver injury was induced in wild-type and egr-1-/- mice by a single injection of carbon tetrachloride (CCl(4)). Liver injury, inflammatory, and hepatoprotective gene expression and signaling events were measured 18, 48, and 72 h after CCl(4) administration.

resultsPeak liver injury was greater in egr-1-/- mice compared to wild-type mice. Enhanced injury in egr-1-/- mice was associated with reduced tumor necrosis factor (TNF)alpha mRNA and protein expression, reduced Akt phosphorylation and nuclear localization of NFkappaB-p65 in nuclei of cells in the hepatic sinusoid. Expression of inducible nitric oxide synthase and cyclooxygenase-2, TNFalpha-regulated genes that have hepatoprotective function, was attenuated in egr-1-/- mice compared to wild-type mice. Although plasma interleukin (IL)-6 protein and hepatic accumulation of IL-6, glycoprotein 130, and IL-6 receptor alpha mRNA in wild-type and egr-1-/- mice were equivalent, signal transducer and activator of transcription 3 phosphorylation was attenuated in egr-1-/- mice and associated with reduced oncostatin M expression.

conclusionsIn contrast to its role in inflammation-mediated tissue injury in other models, Egr-1 expression promotes protection in the liver after CCl(4) exposure.

Indexed as

AnimalsCarbon TetrachlorideDisease Models, AnimalEarly Growth Response Protein 1FemaleGene ExpressionLiver Failure, AcuteMiceMice, Inbred C57BLSignal TransductionCarbon TetrachlorideEarly Growth Response Protein 1

Identifiers

PMID20615570
PMCPMC2930032
OpenAlexW2139259057

What OpenQuestion holds

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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.