Evidence map›Paper›PMID 25012660›Full record

ArticleThe Journal of biological chemistry2014

β-Arrestin 2 negatively regulates Toll-like receptor 4 (TLR4)-triggered inflammatory signaling via targeting p38 MAPK and interleukin 10.

Hui Li, Dan Hu, Huimin Fan, Ying Zhang, Gene D LeSage, Yi Caudle, Charles Stuart, Zhongmin Liu, Deling Yin

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
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  16. GABAPsychopharmacology · 2019
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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.

Hui LiDepartment of Internal Medicine, College of Medicine, East Tennessee State University, Johnson City, Tennessee 37614.
Dan HuDepartment of Internal Medicine, College of Medicine, East Tennessee State University, Johnson City, Tennessee 37614,; Department of Neurology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Huimin FanDepartment of Cardiovascular and Thoracic Surgery, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China, and.
Ying ZhangDepartment of Molecular Microbiology and Immunology, Johns Hopkins University, Baltimore, Maryland 21205.
Gene D LeSageDepartment of Internal Medicine, College of Medicine, East Tennessee State University, Johnson City, Tennessee 37614.
Yi CaudleDepartment of Internal Medicine, College of Medicine, East Tennessee State University, Johnson City, Tennessee 37614.
Charles StuartDepartment of Internal Medicine, College of Medicine, East Tennessee State University, Johnson City, Tennessee 37614.
Zhongmin LiuDepartment of Cardiovascular and Thoracic Surgery, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China, and. Electronic address: zhongmin_liu@sina.com.
Deling YinDepartment of Internal Medicine, College of Medicine, East Tennessee State University, Johnson City, Tennessee 37614,. Electronic address: yin@etsu.edu.
East Tennessee State University · USShanghai East Hospital · CNJohns Hopkins University · US

Funding

PHS HHS NIDA020120PHS HHS NIGM094740
6 · The paper itself

Abstract

The control of IL-10 production in Toll-like receptor (TLR) signals remains to be elucidated. Here, we report that β-arrestin 2 positively regulates TLR-triggered IL-10 production in a p38 mitogen-activated protein kinase (MAPK)-dependent mechanism. In vitro studies with cells including peritoneal macrophages and HEK293/TLR4 cells have demonstrated that β-arrestin 2 forms complexes with p38 and facilitates p38 activation after lipopolysaccharide (LPS) stimulation. Deficiency of β-arrestin 2 and inhibition of p38 MAPK activity both ameliorate TLR4-stimulated IL-10 response. Additionally, in vivo experiments show that mice lacking β-arrestin 2 produce less amount of IL-10, and are more susceptible to LPS-induced septic shock which is further enhanced by blocking IL-10 signal. These results reveal a novel mechanism by which β-arrestin 2 negatively regulates TLR4-mediated inflammatory reactions.

Indexed as

MAP Kinase Signaling SystemAnimalsArrestinsbeta-Arrestin 2beta-ArrestinsHEK293 CellsHumansInflammationInterleukin-10LipopolysaccharidesMacrophages, PeritonealMiceMice, Knockoutp38 Mitogen-Activated Protein KinasesShock, SepticToll-Like Receptor 4ARRB2 protein, humanArrb2 protein, mouseArrestinsbeta-Arrestin 2beta-ArrestinsIL10 protein, mouseInterleukin-10Lipopolysaccharidesp38 Mitogen-Activated Protein KinasesTlr4 protein, mouseToll-Like Receptor 4Cell SignalingEndotoxic ShockIL-10Inflammationp38Protein KinaseToll-like Receptor (TLR)β-Arrestin 2

Identifiers

PMID25012660
PMCPMC4132806
OpenAlexW1978521856

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.