Evidence map›Paper›PMID 18182393›Full record

ArticleThe Journal of biological chemistry2008

JunD protects the liver from ischemia/reperfusion injury by dampening AP-1 transcriptional activation.

Jennifer J Marden, Yulong Zhang, Fredrick D Oakley, Weihong Zhou, Meihui Luo, Hong Peng Jia, Paul B McCray, Moshe Yaniv, Jonathan B Weitzman, John F Engelhardt

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

14 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  4. Attenuation of pulmonary ACE2 activity impairs inactivation of des-ArgAmerican journal of physiology. Lung cellular and molecular physiology · 2018
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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

10 authors at 3 institutions in 2 countries.

Jennifer J MardenMolecular and Cellular Biology Interdisciplinary Graduate Program, University of Iowa College of Medicine, Iowa City, Iowa 52242, USA.
Yulong Zhang
Fredrick D Oakley
Weihong Zhou
Meihui Luo
Hong Peng Jia
Paul B McCray
Moshe Yaniv
Jonathan B Weitzman
John F Engelhardt
University of Iowa · USInserm · FRInstitut Pasteur · FR

Funding

Vector Core-Core 2P30DK054759 · NIDDK · UNIVERSITY OF IOWA · PI Alejandro Antonio Pezzulo · 1998 to 2026
$30.5M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007337 · NIGMS · UNIVERSITY OF IOWA · PI GEYER, PAMELA K., LENTZ, STEVEN R · 1985 to 2020
$15.9M
Redox Mechanisms of Ischemia Reperfusion Injury in the LiverR01DK051315 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI ENGELHARDT, JOHN F · 1996 to 2013
$2.7M
Redox-mediated NF-kappaB activation by LPS and IL-1R01DK067928 · NIDDK · UNIVERSITY OF IOWA · PI ENGELHARDT, JOHN F · 2004 to 2008
$1.4M
NIDDK NIH HHS DK067928NIDDK NIH HHS DK51315NIDDK NIH HHS DK54759NIDDK NIH HHS P30 DK054759NIDDK NIH HHS R01 DK051315NIDDK NIH HHS R01 DK067928NIGMS NIH HHS T32 GM007337
6 · The paper itself

Abstract

The AP-1 transcription factor modulates a wide range of cellular processes, including cellular proliferation, programmed cell death, and survival. JunD is a major component of the AP-1 complex following liver ischemia/reperfusion (I/R) injury; however, its precise function in this setting remains unclear. We investigated the functional significance of JunD in regulating AP-1 transcription following partial lobar I/R injury to the liver, as well as the downstream consequences for hepatocellular remodeling. Our findings demonstrate that JunD plays a protective role, reducing I/R injury to the liver by suppressing acute transcriptional activation of AP-1. In the absence of JunD, c-Jun phosphorylation and AP-1 activation in response to I/R injury were elevated, and this correlated with increased caspase activation, injury, and alterations in hepatocyte proliferation. The expression of dominant negative JNK1 inhibited c-Jun phosphorylation, AP-1 activation, and hepatic injury following I/R in JunD-/- mice but, paradoxically, led to an enhancement of AP-1 activation and liver injury in JunD+/- littermates. Enhanced JunD/JNK1-dependent liver injury correlated with the acute induction of diphenylene iodonium-sensitive NADPH-dependent superoxide production by the liver following I/R. In this context, dominant negative JNK1 expression elevated both Nox2 and Nox4 mRNA levels in the liver in a JunD-dependent manner. These findings suggest that JunD counterbalances JNK1 activation and the downstream redox-dependent hepatic injury that results from I/R, and may do so by regulating NADPH oxidases.

Indexed as

Genes, junTranscriptional ActivationAnimalsCell ProliferationGenes, DominantHepatocytesLiverMembrane GlycoproteinsMiceMice, TransgenicMitogen-Activated Protein Kinase 8Models, BiologicalNADPH Oxidase 2NADPH Oxidase 4NADPH OxidasesProto-Oncogene ProteinsCybb protein, mousejunD protein, mouseMembrane GlycoproteinsMitogen-Activated Protein Kinase 8NADPH Oxidase 2NADPH Oxidase 4NADPH OxidasesNox4 protein, mouseProto-Oncogene ProteinsProto-Oncogene Proteins c-junTranscription Factor AP-1

Identifiers

PMID18182393
PMCPMC3593645
OpenAlexW2019910574

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.