Evidence map›Paper›PMID 28383060›Full record

ArticleScientific reports2017

Phosphodiesterase 4B negatively regulates endotoxin-activated interleukin-1 receptor antagonist responses in macrophages.

Jing-Xing Yang, Kou-Chou Hsieh, Yi-Ling Chen, Chien-Kuo Lee, Marco Conti, Tsung-Hsien Chuang, Chin-Pyng Wu, S-L Catherine Jin

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

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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

8 authors at 5 institutions in 2 countries.

Jing-Xing YangDepartment of Life Sciences, National Central University, Zhongli District, Taoyuan City, Taiwan, Republic of China.
Kou-Chou HsiehInternal Medicine, Landseed Hospital, Pingzhen District, Taoyuan City, Taiwan, Republic of China.
Yi-Ling ChenDepartment of Life Sciences, National Central University, Zhongli District, Taoyuan City, Taiwan, Republic of China.
Chien-Kuo LeeGraduate Institute of Immunology, National Taiwan University College of Medicine, Taipei, Taiwan, Republic of China.
Marco ContiDepartment of Obstetrics, Gynecology, and Reproductive Sciences, University of California San Francisco, California, USA.
Tsung-Hsien ChuangImmunology Research Center, National Health Research Institutes, Miaoli, Taiwan, Republic of China.
Chin-Pyng WuInternal Medicine, Landseed Hospital, Pingzhen District, Taoyuan City, Taiwan, Republic of China.
S-L Catherine JinDepartment of Life Sciences, National Central University, Zhongli District, Taoyuan City, Taiwan, Republic of China.
National Central University · TWLandseed Hospital · TWNational Health Research Institutes · TWNational Taiwan University · TWUniversity of California, San Francisco · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of TLR4 by lipopolysaccharide (LPS) induces both pro-inflammatory and anti-inflammatory cytokine production in macrophages. Type 4 phosphodiesterases (PDE4) are key cAMP-hydrolyzing enzymes, and PDE4 inhibitors are considered as immunosuppressors to various inflammatory responses. We demonstrate here that PDE4 inhibitors enhance the anti-inflammatory cytokine interleukin-1 receptor antagonist (IL-1Ra) secretion in LPS-activated mouse peritoneal macrophages, and this response was regulated at the transcriptional level rather than an increased IL-1Ra mRNA stability. Studies with PDE4-deficient macrophages revealed that the IL-1Ra upregulation elicited by LPS alone is PKA-independent, whereas the rolipram-enhanced response was mediated by inhibition of only PDE4B, one of the three PDE4 isoforms expressed in macrophages, and it requires PKA but not Epac activity. However, both pathways activate CREB to induce IL-1Ra expression. PDE4B ablation also promoted STAT3 phosphorylation (Tyr

Indexed as

AnimalsCell SurvivalCyclic AMPCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinCyclic Nucleotide Phosphodiesterases, Type 4Interleukin-1betaInterleukin 1 Receptor Antagonist ProteinLipopolysaccharidesMacrophages, PeritonealMiceMice, Inbred C57BLPhosphodiesterase 4 InhibitorsPhosphorylationRAW 264.7 CellsRNA, MessengerCyclic AMPCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinCyclic Nucleotide Phosphodiesterases, Type 4Interleukin-1betaInterleukin 1 Receptor Antagonist ProteinLipopolysaccharidesPhosphodiesterase 4 InhibitorsRNA, MessengerRolipramSTAT3 Transcription Factor

Identifiers

PMID28383060
PMCPMC5382768
OpenAlexW2604475574

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.