Evidence map›Paper›PMID 23422584›Full record

ArticleCellular signalling2013

MCPIP1 negatively regulates toll-like receptor 4 signaling and protects mice from LPS-induced septic shock.

Shengping Huang, Ruidong Miao, Zhou Zhou, Tianyi Wang, Jianguo Liu, Gang Liu, Y Eugene Chen, Hong-Bo Xin, Jifeng Zhang, Mingui Fu

Abstract read
In one paragraph

Article in Cellular signalling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Roquin-1 interaction with Regnase-1 inhibits the progression of rheumatoid arthritis via suppressing FGF2 expression and NF-κB pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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  18. Tim-4 protects mice against lipopolysaccharide-induced endotoxic shock by suppressing the NF-κB signaling pathway.Laboratory investigation; a journal of technical methods and pathology · 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

10 authors at 6 institutions in 2 countries.

Shengping HuangDepartment of Basic Medical Science, School of Medicine, University of Missouri Kansas City, Kansas City, MO 64108, USA.
Ruidong Miao
Zhou Zhou
Tianyi Wang
Jianguo Liu
Gang Liu
Y Eugene Chen
Hong-Bo Xin
Jifeng Zhang
Mingui Fu
University of Michigan–Ann Arbor · USUniversity of Missouri–Kansas City · USNanchang University · CNSaint Louis University · USUniversity of Alabama at Birmingham · USUniversity of Pittsburgh · US

Funding

The Role of PPAR-gamma in Vascular Lesion FormationR01HL068878 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2002 to 2019
$7.6M
Urokinase, Neutrophil Activation and Acute Lung Injury.R01HL076206 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI LIU, GANG · 2005 to 2013
$2.8M
Nitroalkenes and Blood Pressure RegulationR01HL089544 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2008 to 2012
$2.0M
The role of tristetraprolin in control of breast cancer progressionR01CA163808 · NCI · SAINT LOUIS UNIVERSITY · PI LIU, JIANGUO · 2012 to 2016
$1.5M
Molecular mechanisms of host-derived CCL5 mediated mammary tumor growthK22CA137126 · NCI · SAINT LOUIS UNIVERSITY · PI LIU, JIANGUO · 2010 to 2012
$515k
The role of MCPIP1 in regulating NF-kB signaling and macrophage activationR21HL098794 · NHLBI · UNIVERSITY OF MISSOURI KANSAS CITY · PI FU, MINGUI · 2011 to 2012
$413k
MicroRNAs, inflammation, and acute lung injury.R21HL097218 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LIU, GANG · 2010 to 2011
$403k
NCI NIH HHS CA137126NCI NIH HHS CA163808NCI NIH HHS K22 CA137126NCI NIH HHS R01 CA163808NHLBI NIH HHS HL068878NHLBI NIH HHS HL076206NHLBI NIH HHS HL089544NHLBI NIH HHS HL097218NHLBI NIH HHS HL098794NHLBI NIH HHS R01 HL068878NHLBI NIH HHS R01 HL076206NHLBI NIH HHS R01 HL089544NHLBI NIH HHS R21 HL097218NHLBI NIH HHS R21 HL098794
6 · The paper itself

Abstract

Septic shock is one of leading causes of morbidity and mortality in hospital patients. However, genetic factors predisposing to septic shock are not fully understood. Our previous work showed that MCP-induced protein 1 (MCPIP1) was induced by lipopolysaccharides (LPSs), which then negatively regulates LPS-induced inflammatory signaling in vitro. Here we report that although MCPIP1 was induced by various toll-like receptor (TLR) ligands in macrophages, MCPIP1-deficient mice are extremely susceptible to TLR4 ligand (LPS)-induced septic shock and death, but not to the TLR2, 3, 5 and 9 ligands-induced septic shock. Consistently, LPS induced tumor necrosis factor α (TNFα) production in MCPIP1-deficient mice was 20-fold greater than that in their wild-type littermates. Further analysis revealed that MCPIP1-deficient mice developed severe acute lung injury after LPS injection and JNK signaling was highly activated in MCPIP1-deficient lungs after LPS stimulation. Finally, macrophage-specific MCPIP1 transgenic mice were partially protected from LPS-induced septic shock, suggesting that inflammatory cytokines from sources other than macrophages may significantly contribute to the pathogenesis of LPS-induced septic shock. Taken together, these results suggest that MCPIP1 selectively suppresses TLR4 signaling pathway and protects mice from LPS-induced septic shock.

Indexed as

Acute Lung InjuryAnimalsCell LineFemaleJNK Mitogen-Activated Protein KinasesLipopolysaccharidesMaleMiceMice, Inbred C57BLMice, KnockoutPhosphorylationRibonucleasesShock, SepticSignal TransductionToll-Like Receptor 4Tumor Necrosis Factor-alphaJNK Mitogen-Activated Protein KinasesLipopolysaccharidesRibonucleasesToll-Like Receptor 4Tumor Necrosis Factor-alphaZc3h12a protein, mouse

Identifiers

PMID23422584
PMCPMC3622792
OpenAlexW1972492206

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Registered trials

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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.