Evidence map›Paper›PMID 28941191›Full record

ArticleCNS neuroscience & therapeutics2017

Activating α7 nicotinic acetylcholine receptor inhibits NLRP3 inflammasome through regulation of β-arrestin-1.

Ping Ke, Bo-Zong Shao, Zhe-Qi Xu, Xiong-Wen Chen, Wei Wei, Chong Liu

Open access · bronzeAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

38 citing papers in PubMed, 51 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

6 authors at 3 institutions in 2 countries.

Ping KeDepartment of Pharmacology, Second Military Medical University, Shanghai, China.ORCID http://orcid.org/0000-0001-9456-9094
Bo-Zong ShaoDepartment of Pharmacology, Second Military Medical University, Shanghai, China.
Zhe-Qi XuDepartment of Pharmacology, Second Military Medical University, Shanghai, China.
Xiong-Wen ChenCardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA, USA.
Wei WeiState Key Laboratory Breeding Base for Zhejiang Sustainable Plant Pest and Disease Control, Zhejiang Province Key Laboratory for Food Safety, Zhejiang Academy of Agricultural Sciences, Institute of Quality and Standard for Agro-products, Hangzhou, China.
Chong LiuDepartment of Pharmacology, Second Military Medical University, Shanghai, China.
Second Military Medical University · CNTemple University · USZheJiang Academy of Agricultural Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsTo evaluate whether activating α7 nicotinic acetylcholine receptor (α7nAChR) could inhibit the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome through regulation of β-arrestin-1 in monocyte/macrophage system, thus contributing to the control of neuroinflammation.

methodsThe protein levels of NLRP3, caspase-1 (Casp-1) p20 and proCasp-1, interleukin-1β (IL-1β) p17 and proIL-1β, IL-18 and proIL-18 were measured using Western blotting. The mRNA levels of Casp-1 and IL-1β were detected by real-time PCR (RT-PCR). The colocalization and interaction of NLRP3 protein and β-arrestin-1 were measured by immunofluorescence staining and immunoprecipitation.

resultsThe expression of β-arrestin-1 was significantly increased and colocalized with CD45-positive cells in spinal cord of experimental auto-immune encephalomyelitis (EAE) mice when compared with the sham mice, which was attenuated by pretreatment with PNU282987, a specific α7nAChR agonist. PNU282987 also significantly inhibited the activation of NLRP3 inflammasome and thus decreased the production of IL-1β and IL-18 both in lipopolysaccharide (LPS)/ATP-stimulated BV2 microglia in vitro and spinal cord from EAE mice in vivo, while inverse effects were observed in α7nAChR knockout mice. Furthermore, overexpression of β-arrestin-1 attenuated the inhibitory effect of PNU282987 on NLRP3 inflammasome activation in LPS/ATP-stimulated BV2 microglia. PNU282987 inhibited the interaction between β-arrestin-1 and NLRP3 protein in vitro.

conclusionsThe present study demonstrates that activating α7nAChR can lead to NLRP3 inflammasome inhibition via regulation of β-arrestin-1 in monocyte/microglia system.

Indexed as

Adenosine Triphosphatealpha7 Nicotinic Acetylcholine ReceptorAnimalsAnti-Inflammatory AgentsBenzamidesbeta-Arrestin 1Bridged Bicyclo CompoundsCaspase 1Cell LineEncephalomyelitis, Autoimmune, ExperimentalInflammasomesInterleukin-18Interleukin-1betaLipopolysaccharidesMice, Inbred C57BLMice, KnockoutAdenosine Triphosphatealpha7 Nicotinic Acetylcholine ReceptorAnti-Inflammatory AgentsArrb1 protein, mouseBenzamidesbeta-Arrestin 1Bridged Bicyclo CompoundsCaspase 1IL1B protein, mouseInflammasomesInterleukin-18Interleukin-1betaLipopolysaccharidesNicotinic AgonistsNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mousePNU-282987neuroinflammationNLRP3 inflammasomeα7nAChRβ-arrestin-1

Identifiers

PMID28941191
PMCPMC6492746
OpenAlexW2759874929

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.