Evidence map›Paper›PMID 31428926›Full record

ArticleNeuroscience bulletin2020

MiR-125a-5p Regulates Vitamin D Receptor Expression in a Mouse Model of Experimental Autoimmune Encephalomyelitis.

Han-Chun Long, Rui Wu, Chun-Feng Liu, Fei-Long Xiong, Zu Xu, Dian He, Yi-Fan Zhang, Bing Shao, Ping-An Zhang, Guang-Yin Xu and 1 more

Open access · greenAbstract read
In one paragraph

Article in Neuroscience bulletin, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  9. The Roles of Orphan G Protein-Coupled Receptors in Autoimmune Diseases.Clinical reviews in allergy & immunology · 2021
    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

11 authors at 4 institutions in 1 country.

Han-Chun LongDepartment of Neurology, The Second Affiliated Hospital of Soochow University, Suzhou, 215008, China.
Rui WuInstitute of Neuroscience, Soochow University, Suzhou, 215123, China.
Chun-Feng LiuDepartment of Neurology, The Second Affiliated Hospital of Soochow University, Suzhou, 215008, China.
Fei-Long XiongDepartment of Neurology, The Second Affiliated Hospital of Soochow University, Suzhou, 215008, China.
Zu XuDepartment of Neurology, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550001, China.
Dian HeDepartment of Neurology, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550001, China.
Yi-Fan ZhangDepartment of Neurology, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550001, China.
Bing ShaoDepartment of Neurology, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550001, China.
Ping-An ZhangInstitute of Neuroscience, Soochow University, Suzhou, 215123, China.
Guang-Yin XuInstitute of Neuroscience, Soochow University, Suzhou, 215123, China. guangyinxu@suda.edu.cn.
Lan ChuDepartment of Neurology, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550001, China. chulan8999@yeah.net.
Soochow University · CNGuiyang Medical University · CNAffiliated Hospital of Guizhou Medical University · CNSecond Affiliated Hospital of Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is a chronic and incurable autoimmune neurodegenerative disease of the central nervous system. Although the symptoms of MS can be managed by vitamin D3 treatment alone, this condition cannot be completely eradicated. Thus, there might be unknown factors capable of regulating the vitamin D receptor (VDR). Genome-wide analysis showed that miRNAs were associated with VDRs. We sought to determine the role and mechanism of action of miRNA-125a-5p and VDRs in a model of MS, mice with experimental autoimmune encephalomyelitis (EAE), which was induced by myelin oligodendrocyte glycoprotein 35-55 peptides. EAE mice showed decreased mean body weight but increased mean clinical scores compared with vehicle or control mice. And inflammatory infiltration was found in the lumbosacral spinal cord of EAE mice. In addition, VDR expression was significantly lower while the expression of miR-125a-5p was markedly higher in the spinal ventral horn of EAE mice than in vehicle or control mice. Importantly, activation of VDRs by paricalcitol or inhibition of miR-125a-5p by its antagomir markedly decreased the mean clinical scores in EAE mice. Interestingly, VDR and miR-125a-5p were co-localized in the same neurons of the ventral horn. More importantly, inhibition of miR-125a-5p remarkably blocked the decrease of VDRs in EAE mice. These results support a critical role for miR-125a-5p in modulating VDR activity in EAE and suggest potential novel therapeutic interventions.

Indexed as

AnimalsEncephalomyelitis, Autoimmune, ExperimentalFemaleLumbosacral RegionMiceMice, Inbred C57BLMicroRNAsMultiple SclerosisReceptors, CalcitriolSpinal Cord Ventral HornMicroRNAsMirn125 microRNA, mouseReceptors, CalcitriolExperimental autoimmune encephalomyelitisMiR-125a-5pMultiple sclerosisMyelin oligodendrocyte glycoprotein 35–55 peptidesVitamin D receptor

Identifiers

PMID31428926
PMCPMC6977816
OpenAlexW2969741346

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.