Evidence map›Paper›PMID 35678979›Full record

ArticleMolecular neurobiology2022

LncRNA ZNF883-Mediated NLRP3 Inflammasome Activation and Epilepsy Development Involve USP47 Upregulation.

Lina Gong, Yaru Han, Ru Chen, Pu Yang, Chen Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  4. Review
  5. LncRNAs Orchestrating Neuroinflammation: A Comprehensive Review.Cellular and molecular neurobiology · 2025
    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

5 authors at 1 institution in 1 country.

Lina GongDepartment of Neurology, the Third Xiangya Hospital of Central South University, No. 138 Tongzipo Road, Yuelu District, Changsha, Hunan, 410013, People's Republic of China.
Yaru HanDepartment of Neurology, the Third Xiangya Hospital of Central South University, No. 138 Tongzipo Road, Yuelu District, Changsha, Hunan, 410013, People's Republic of China.
Ru ChenDepartment of Neurology, the Third Xiangya Hospital of Central South University, No. 138 Tongzipo Road, Yuelu District, Changsha, Hunan, 410013, People's Republic of China.
Pu YangDepartment of Neurology, the Third Xiangya Hospital of Central South University, No. 138 Tongzipo Road, Yuelu District, Changsha, Hunan, 410013, People's Republic of China.
Chen ZhangDepartment of Neurology, the Third Xiangya Hospital of Central South University, No. 138 Tongzipo Road, Yuelu District, Changsha, Hunan, 410013, People's Republic of China. zhangchen198212@126.com.ORCID http://orcid.org/0000-0003-2955-4501
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The goal of this study was to characterize the mechanisms of long noncoding RNA (lncRNA) ZNF883 regulating NOD-like receptor 3 (NLRP3) inflammasome activation in epilepsy (EP). Rat and cellular EP models were established using pilocarpine and magnesium-free extracellular fluid, respectively, to detect the differential expression of ZNF883, microRNA (miR)-138-5p, ubiquitin-specific peptidase 47 (USP47), and NLRP3. The pathology of the hippocampal neurons was examined by whole-cell patch clamping. The expression of ZNF883, miR-138-5p, and USP47 was modified in epileptic neurons, and the EP rats were injected with sh-ZNF883. Then, alterations in ZNF883, miR-138-5p, and USP47 levels were measured. The histopathology of the hippocampus was detected, along with the detection of IL-6, IL-1β, TNF-α, and NLRP3. Neuronal apoptosis in the rat and cellular EP models was determined. The relationship among ZNF883, miR-138-5p, and USP47 as well as the regulation of NLRP3 ubiquitination by USP47 was determined. ZNF883, USP47, and NLRP3 were increasingly expressed and miR-138-5p was downregulated in epileptic neurons and rats, concurrent with aggravated inflammation and apoptosis. ZNF883 overexpression in epileptic neurons elevated USP47 expression. ZNF883 targeted miR-138-5p and miR-138-5p negatively regulated USP47. In epileptic neurons, inhibiting miR-138-5p or overexpressing USP47 partially reversed the ZNF883 silencing-induced inhibition on NLRP3 inflammasome activation, neuronal apoptosis, and epileptiform activity. ZNF883 silencing in EP rats decreased USP47 and NLRP3, increased miR-138-5p, and inhibited inflammation and apoptosis. USP47 reversed the ubiquitination of NLRP3. ZNF883 inhibits NLRP3 ubiquitination and promotes EP through upregulating USP47 by sponging miR-138-5p.

Indexed as

EpilepsyMicroRNAsRNA, Long NoncodingUbiquitin-Specific ProteasesUbiquitin ThiolesteraseAnimalsApoptosisInflammasomesInflammationNLR Family, Pyrin Domain-Containing 3 ProteinNLR ProteinsRatsUp-RegulationInflammasomesMicroRNAsMIRN138 microRNA, ratNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratNLR ProteinsRNA, Long NoncodingUbiquitin-Specific ProteasesUbiquitin ThiolesteraseUsp47 protein, ratEpilepsyLong noncoding RNA ZNF883miR-138-5pNLRP3UbiquitinationUSP47

Identifiers

PMID35678979
OpenAlexW4281788844

What Socratic 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 Socratic graph.