Evidence map›Paper›PMID 33013847›Full record

ArticleFrontiers in immunology2020

Mechanisms of M2 Macrophage-Derived Exosomal Long Non-coding RNA PVT1 in Regulating Th17 Cell Response in Experimental Autoimmune Encephalomyelitisa.

Lei Wu, Jinjin Xia, Donghui Li, Ying Kang, Wei Fang, Peng Huang

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-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

24 citing papers in PubMed, 31 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Lei WuDepartment of Neurology, The Second Affiliated Hospital of Zhejiang, University School of Medicine, Hangzhou, China.
Jinjin XiaDepartment of Neurology, Changxing Hospital, Second Affiliated Hospital of Medical College of Zhejiang University, Huzhou, China.
Donghui LiDepartment of Neurology, Changxing Hospital, Second Affiliated Hospital of Medical College of Zhejiang University, Huzhou, China.
Ying KangDepartment of Pollution Source Statistics, Zhejiang Provincial Environmental Monitoring Center, Hangzhou, China.
Wei FangSchool of Pharmacy, Anhui University of Traditional Chinese Medicine, Hefei, China.
Peng HuangSchool of Pharmacy, Anhui University of Traditional Chinese Medicine, Hefei, China.
Second Affiliated Hospital of Zhejiang University · CNAnhui University of Traditional Chinese Medicine · CNZhejiang Environmental Monitoring Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNA (lncRNA) is pivotal for multiple sclerosis (MS), but the potential mechanism of lncRNA PVT1 in MS animal model, experimental autoimmune encephalomyelitis (EAE) still remains unclear. In this study, macrophages were firstly isolated and induced to polarize into M2 macrophages. M2 macrophage-derived exosomes (M2-exos) were extracted and identified, and EAE mouse model was established and treated with M2-exos. The effect of M2-exos on EAE mice was evaluated by clinical scores. The proportion of Treg and Th17 cells in spinal cord cells and splenocytes, and levels of inflammatory factors were measured. The targeting relationships among PVT1, miR-21-5p, and SOCS5 were verified. The expression of JAKs/STAT3 pathway-related proteins was measured. After M2-exo treatment, the clinical score of EAE mice decreased, and demyelination and inflammatory infiltration improved; Th17 cells decreased, Treg cells increased, and the levels of inflammatory factors decreased significantly. SOCS5 and PVT1 were downregulated and miR-21-5p was upregulated in EAE mice. PVT1 could sponge miR-21-5p to regulate SOCS5. SOCS5 alleviated EAE symptoms by repressing the JAKs/STAT3 pathway. Together, M2-exos-carried lncRNA PVT1 sponged miR-21-5p to upregulate SOCS5 and inactivate the JAKs/STAT3 pathway, thus reducing inflammation and protecting EAE mice. This study may offer novel treatments for MS.

Indexed as

AnimalsCells, CulturedEncephalomyelitis, Autoimmune, ExperimentalExosomesJanus KinasesMacrophages, PeritonealMiceMice, Inbred C57BLMicroRNAsPhenotypeRNA, Long NoncodingSignal TransductionSpinal CordSpleenSTAT3 Transcription FactorSuppressor of Cytokine Signaling ProteinsJanus KinasesMicroRNAsMIRN21 microRNA, mousePVT1 long-non-coding RNA, mouseRNA, Long NoncodingSocs5 protein, mouseStat3 protein, mouseSTAT3 Transcription FactorSuppressor of Cytokine Signaling Proteinsexosomesexperimental autoimmune encephalomyelitislong non-coding RNA PVT1M2 macrophagesmicroRNA-21-5pSOCS5

Identifiers

PMID33013847
PMCPMC7500097
OpenAlexW3083628463

What OpenQuestion holds

Textmetadata
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.