Evidence map›Paper›PMID 33184298›Full record

ArticleScientific reports2020

Knockdown lncRNA NEAT1 regulates the activation of microglia and reduces AKT signaling and neuronal apoptosis after cerebral ischemic reperfusion.

Xunran Ni, Qian Su, Wenbo Xia, Yanli Zhang, Kejuan Jia, Zhiqiang Su, Guozhong Li

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
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  16. LncRNAsNon-coding RNA research · 2023
    Article
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  18. Article
  19. Regulation of microglia polarization after cerebral ischemia.Frontiers in cellular neuroscience · 2023
    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

7 authors at 2 institutions in 1 country.

Xunran NiThe First Affiliated Hospital of Harbin Medical University, Harbin, 150001, People's Republic of China.
Qian SuThe First Affiliated Hospital of Harbin Medical University, Harbin, 150001, People's Republic of China.
Wenbo XiaThe First Affiliated Hospital of Harbin Medical University, Harbin, 150001, People's Republic of China.
Yanli ZhangThe First Affiliated Hospital of Harbin Medical University, Harbin, 150001, People's Republic of China.
Kejuan JiaThe First Affiliated Hospital of Harbin Medical University, Harbin, 150001, People's Republic of China.
Zhiqiang SuThe First Affiliated Hospital of Harbin Medical University, Harbin, 150001, People's Republic of China. suzhiqiang2020@126.com.
Guozhong LiThe First Affiliated Hospital of Harbin Medical University, Harbin, 150001, People's Republic of China. lgzhyd1962@163.com.
First Affiliated Hospital of Harbin Medical University · CNHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute cerebral ischaemia may lead to serious consequences, including brain injury caused by uncontrolled reperfusion, which occurs when circulation is re-established. The long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) plays an important role in the immune system. However, the potential roles and underlying molecular mechanisms of NEAT1 in cerebral ischaemia/reperfusion (I/R) injury remain unclear. The aim of the present study was to investigate the function of the lncRNA NEAT1 in cerebral I/R injury and its potential beneficial effects on neurons. In our study, oxygen-glucose deprivation (OGD)/reoxygenation (OGD/R) was induced in vitro to mimic cerebral I/R injury. Cholecystokinin-octopeptide (CCK-8) was used to measure cell viability, and flow cytometry was used to measure cell apoptosis. Real-time quantitative PCR (qRT-PCR) was used to measure the expression of phenotypic markers of classically activated (M1) and alternatively activated (M2) microglia, and western blotting was performed to detect the levels of proteins related to the AKT/STAT3 pathway. The expression of the lncRNA NEAT1 was significantly upregulated in patients with ischaemic stroke, and knockdown of the lncRNA NEAT1 alleviated OGD/R-induced apoptosis and increased neuronal viability. Furthermore, the lncRNA NEAT1 may inhibit microglial polarization towards the M1 phenotype to reduce the damage caused by OGD/R and reduce the activity of the AKT/STAT3 pathway. In conclusion, the lncRNA NEAT1 may be a potential target for new therapeutic interventions for cerebral I/R.

Indexed as

ApoptosisBrain IschemiaCell PolarityCells, CulturedDrug Delivery SystemsFlow CytometryGlucoseHumansInflammationMicrogliaNeuronsOxygenProto-Oncogene Proteins c-aktRNA, Long NoncodingSignal TransductionSTAT3 Transcription FactorGlucoseNEAT1 long non-coding RNA, humanOxygenProto-Oncogene Proteins c-aktRNA, Long NoncodingSTAT3 Transcription Factor

Identifiers

PMID33184298
PMCPMC7665206
OpenAlexW3098632814

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Registered trials

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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.