Evidence map›Paper›PMID 32723328›Full record

ArticleJournal of neuroinflammation2020

NF-κB p65-dependent transcriptional regulation of histone deacetylase 2 contributes to the chronic constriction injury-induced neuropathic pain via the microRNA-183/TXNIP/NLRP3 axis.

Jiamin Miao, Xuelong Zhou, Tianjiao Ji, Gang Chen

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

Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
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  6. The role of non-coding RNAs in neuropathic pain.Pflugers Archiv : European journal of physiology · 2024
    Review
  7. Article
  8. Pathology of pain and its implications for therapeutic interventions.Signal transduction and targeted therapy · 2024
    Review
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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

4 authors at 3 institutions in 2 countries.

Jiamin MiaoDepartment of Anesthesiology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, No. 3, Qingchun East Road, Jianggan District, Hangzhou, 310012, Zhejiang Province, China. jmmiao@zju.edu.cn.
Xuelong ZhouDepartment of Anesthesiology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, China.
Tianjiao JiLaboratory for Biomaterials and Drug Delivery, Department of Anesthesiology, Boston Children's Hospital, Harvard Medical School, Boston, 02115, USA.
Gang ChenDepartment of Anesthesiology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, No. 3, Qingchun East Road, Jianggan District, Hangzhou, 310012, Zhejiang Province, China. chengang120@zju.edu.cn.
Sir Run Run Shaw Hospital · CNHarvard University · USZhejiang University · CN

Funding

Natural Science Foundation of Zhejiang Province No. LY16H090008
6 · The paper itself

Abstract

backgroundNeuropathic pain is related to the sustained activation of neuroglial cells and the production of proinflammatory cytokines in the spinal dorsal horn. However, the clinical efficacy of currently available treatments is very limited. The transcription factor nuclear factor κB (NF-κB) is a ubiquitously expressed protein family and considered to be crucial in autoimmunity. Thus, our study aimed to examine the influence of NF-κB p65 in chronic constriction injury (CCI)-induced neuropathic pain as well as its underlying mechanism.

methodsA rat model of neuropathic pain was established by CCI induction followed by isolation of microglial cells. The binding of NF-κB p65 to HDAC2, of miR-183 to TXNIP, and of TXNIP to NLRP3 was investigated. Expression of miR-183, NF-κB p65, HDAC2, TXNIP, and NLRP3 was determined with their functions in CCI rats and microglial cells analyzed by gain- and loss-of-function experiments.

resultsNF-κB p65 and HDAC2 were upregulated while miR-183 was downregulated in the dorsal horn of the CCI rat spinal cord. NF-κB p65 was bound to the HDAC2 promoter and then increased its expression. HDAC2 reduced miR-183 expression by deacetylation of histone H4. Additionally, miR-183 negatively regulated TXNIP. Mechanistically, NF-κB p65 downregulated the miR-183 expression via the upregulation of HDAC2 and further induced inflammatory response by activating the TXNIP-NLRP3 inflammasome axis, thus aggravating the neuropathic pain in CCI rats and microglial cells.

conclusionThese results revealed a novel transcriptional mechanism of interplay between NF-κB and HDAC2 focusing on neuropathic pain via the miR-183/TXNIP/NLRP3 axis.

Indexed as

AnimalsCell Cycle ProteinsConstriction, PathologicGene Expression RegulationHistone Deacetylase 2LigationMaleMicroRNAsNeuralgiaNLR Family, Pyrin Domain-Containing 3 ProteinRatsRats, Sprague-DawleySciatic NerveSignal TransductionTranscription Factor RelACell Cycle ProteinsHdac2 protein, ratHistone Deacetylase 2MicroRNAsMIRN183 microRNA, ratNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratRela protein, ratTranscription Factor RelATXNIP protein, ratChronic constriction injuryHistone deacetylase 2microRNA-183Neuropathic painNF-κB p65NLRP3TXNIP

Identifiers

PMID32723328
PMCPMC7389436
OpenAlexW3045515178

What OpenQuestion holds

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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.