Evidence map›Paper›PMID 26472924›Full record

ArticleThe Journal of biological chemistry2015

The Nogo/Nogo Receptor (NgR) Signal Is Involved in Neuroinflammation through the Regulation of Microglial Inflammatory Activation.

Yinquan Fang, Jun Yan, Chenhui Li, Xiao Zhou, Lemeng Yao, Tao Pang, Ming Yan, Luyong Zhang, Lei Mao, Hong Liao

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed, 39 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

10 authors at 3 institutions in 2 countries.

Yinquan FangFrom the Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, 24 Tongjiaxiang Street, Nanjing 210009, China.
Jun YanFrom the Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, 24 Tongjiaxiang Street, Nanjing 210009, China.
Chenhui LiFrom the Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, 24 Tongjiaxiang Street, Nanjing 210009, China.
Xiao Zhouthe Department of Biophysics, Saarland University, Homburg 66421, Germany, and.
Lemeng YaoFrom the Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, 24 Tongjiaxiang Street, Nanjing 210009, China.
Tao PangFrom the Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, 24 Tongjiaxiang Street, Nanjing 210009, China.
Ming YanFrom the Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, 24 Tongjiaxiang Street, Nanjing 210009, China.
Luyong ZhangFrom the Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, 24 Tongjiaxiang Street, Nanjing 210009, China.
Lei Maothe Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing 210002, China leiching@163.com.
Hong LiaoFrom the Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, 24 Tongjiaxiang Street, Nanjing 210009, China, hliao@cpu.edu.cn.
China Pharmaceutical University · CNNanjing General Hospital of Nanjing Military Command · CNSaarland University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglia have been proposed to play a pivotal role in the inflammation response of the CNS by expressing a range of proinflammatory enzymes and cytokines under pathological stimulus. Our previous study has confirmed that Nogo receptor (NgR), an axon outgrowth inhibition receptor, is also expressed on microglia and regulates cell adhesion and migration behavior in vitro. In the present study, we further investigated the proinflammatory effects and possible mechanisms of Nogo on microglia in vitro. In this study, Nogo peptide, Nogo-P4, a 25-amino acid core inhibitory peptide sequence of Nogo-66, was used. We found that Nogo-P4 was able to induce the expression of inducible nitric-oxide synthase and cyclooxygenase-2 and the release of proinflammatory cytokines, including IL-1β, TNF-α, NO, and prostaglandin E2 in microglia, which could be reversed by NEP1-40 (Nogo-66(1-40) antagonist peptide), phosphatidylinositol-specificphospholipase C, or NgR siRNA treatment. After Nogo-P4 stimulated microglia, the phosphorylation levels of NF-κB and STAT3 were increased obviously, which further mediated microglia expressing proinflammatory factors induced by Nogo-P4. Taken together, we concluded that Nogo peptide could directly take part in CNS inflammatory process by influencing the expression of proinflammatory factors in microglia, which were related to the NF-κB and STAT3 signal pathways. Besides neurite outgrowth restriction, the Nogo/NgR signal might be involved in multiple processes in various inflammation-associated CNS diseases.

Indexed as

Signal TransductionAnimalsCell LineCyclooxygenase 2DinoprostoneGPI-Linked ProteinsInflammationInterleukin-1betaMiceMicrogliaMyelin ProteinsNF-kappa BNitric OxideNogo ProteinsNogo Receptor 1RatsCyclooxygenase 2DinoprostoneGPI-Linked ProteinsIL1B protein, mouseIL1B protein, ratInterleukin-1betaMyelin ProteinsNF-kappa BNitric OxideNogo ProteinsNogo Receptor 1Ptgs2 protein, mousePtgs2 protein, ratReceptors, Cell SurfaceRtn4 protein, mouseRtn4 protein, ratRtn4r protein, ratStat3 protein, mouseStat3 protein, ratSTAT3 Transcription FactorTumor Necrosis Factor-alphamicroglianeurodegenerative diseaseneuroinflammationNF-kappaBNgRNogo peptideSTAT3

Identifiers

PMID26472924
PMCPMC4661404
OpenAlexW2278557375

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.