Evidence map›Paper›PMID 28717866›Full record

ArticleNeuroscience bulletin2017

MiR-30a Positively Regulates the Inflammatory Response of Microglia in Experimental Autoimmune Encephalomyelitis.

Xue Fang, Dingya Sun, Zhihong Wang, Zhongwang Yu, Weili Liu, Yingyan Pu, Dan Wang, Aijun Huang, Mingdong Liu, Zhenghua Xiang and 2 more

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

Article in Neuroscience bulletin, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.3field-weighted citation impact, top 7% 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, 35 citations in OpenAlex.

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  14. Environmental Influencers, MicroRNA, and Multiple Sclerosis.Journal of central nervous system disease · 2020
    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

12 authors at 1 institution in 1 country.

Xue FangKey Laboratory of Molecular Neurobiology of the Ministry of Education and the Collaborative Innovation Center for Brain Science, Institute of Neuroscience, Second Military Medical University, Shanghai, 200433, China.
Dingya SunKey Laboratory of Molecular Neurobiology of the Ministry of Education and the Collaborative Innovation Center for Brain Science, Institute of Neuroscience, Second Military Medical University, Shanghai, 200433, China.
Zhihong WangKey Laboratory of Molecular Neurobiology of the Ministry of Education and the Collaborative Innovation Center for Brain Science, Institute of Neuroscience, Second Military Medical University, Shanghai, 200433, China.
Zhongwang YuKey Laboratory of Molecular Neurobiology of the Ministry of Education and the Collaborative Innovation Center for Brain Science, Institute of Neuroscience, Second Military Medical University, Shanghai, 200433, China.
Weili LiuKey Laboratory of Molecular Neurobiology of the Ministry of Education and the Collaborative Innovation Center for Brain Science, Institute of Neuroscience, Second Military Medical University, Shanghai, 200433, China.
Yingyan PuKey Laboratory of Molecular Neurobiology of the Ministry of Education and the Collaborative Innovation Center for Brain Science, Institute of Neuroscience, Second Military Medical University, Shanghai, 200433, China.
Dan WangKey Laboratory of Molecular Neurobiology of the Ministry of Education and the Collaborative Innovation Center for Brain Science, Institute of Neuroscience, Second Military Medical University, Shanghai, 200433, China.
Aijun HuangKey Laboratory of Molecular Neurobiology of the Ministry of Education and the Collaborative Innovation Center for Brain Science, Institute of Neuroscience, Second Military Medical University, Shanghai, 200433, China.
Mingdong LiuKey Laboratory of Molecular Neurobiology of the Ministry of Education and the Collaborative Innovation Center for Brain Science, Institute of Neuroscience, Second Military Medical University, Shanghai, 200433, China.
Zhenghua XiangKey Laboratory of Molecular Neurobiology of the Ministry of Education and the Collaborative Innovation Center for Brain Science, Institute of Neuroscience, Second Military Medical University, Shanghai, 200433, China.
Cheng HeKey Laboratory of Molecular Neurobiology of the Ministry of Education and the Collaborative Innovation Center for Brain Science, Institute of Neuroscience, Second Military Medical University, Shanghai, 200433, China. chenghe@smmu.edu.cn.
Li CaoKey Laboratory of Molecular Neurobiology of the Ministry of Education and the Collaborative Innovation Center for Brain Science, Institute of Neuroscience, Second Military Medical University, Shanghai, 200433, China. caoli@smmu.edu.cn.
Second Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is a classical inflammatory demyelinating disease of the central nervous system (CNS). Microglia are the main resident immune cells in the CNS and are closely associated with the pathogenesis of MS. In the present study, we found that miR-30a was highly expressed in jellyfish-like microglia in chronic active lesions of MS patients, as well as in the microglia of mice with experimental autoimmune encephalomyelitis (EAE) at the chronic phase. In vitro, the conditioned supernatant of mouse microglia overexpressing miR-30a promoted the apoptosis of oligodendrocyte precursor cells (OPCs), and inhibited OPC differentiation. In vivo, overexpressing miR-30a in transplanted microglia exacerbated the progression of EAE. Overexpression and knock-down experiments in primary cultured mouse microglia showed that miR-30a increased the expression of IL-1β and iNOS, which are pro-inflammatory, while inhibiting the expression of Ym-1 and CD206. Mechanistically, miR-30a inhibited the expression of Ppargc1b, which is the co-activator of peroxisome proliferator-activated receptor gamma, resulting in pro-inflammatory effects. Our work shows that miR-30a is an important regulator of the inflammatory response in microglia, and may be a promising therapeutic target for inflammatory diseases like MS in the CNS.

Indexed as

AnimalsAnimals, NewbornCells, CulturedEncephalomyelitis, Autoimmune, ExperimentalHumansMiceMice, Inbred C57BLMicrogliaMicroRNAsMultiple SclerosisOligodendrocyte Precursor CellsRatsRats, Sprague-DawleyMicroRNAsMIRN30b microRNA, humanMirn30d microRNA, mouseExperimental autoimmune encephalomyelitisInflammationMicrogliaMiR-30aMultiple sclerosis

Identifiers

PMID28717866
PMCPMC5725374
OpenAlexW2734465458

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.