Evidence map›Paper›PMID 25183005›Full record

ArticleThe Journal of biological chemistry2014

Interleukin-17 (IL-17)-induced microRNA 873 (miR-873) contributes to the pathogenesis of experimental autoimmune encephalomyelitis by targeting A20 ubiquitin-editing enzyme.

Xiaomei Liu, Fengxia He, Rongrong Pang, Dan Zhao, Wen Qiu, Kai Shan, Jing Zhang, Yanlai Lu, Yan Li, Yingwei Wang

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

44 citing papers in PubMed, 90 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Xiaomei LiuFrom the Department of Microbiology and Immunology, Nanjing Medical University, Hanzhong Road 140, Nanjing, Jiangsu 210029, China.
Fengxia HeFrom the Department of Microbiology and Immunology, Nanjing Medical University, Hanzhong Road 140, Nanjing, Jiangsu 210029, China.
Rongrong PangFrom the Department of Microbiology and Immunology, Nanjing Medical University, Hanzhong Road 140, Nanjing, Jiangsu 210029, China.
Dan ZhaoFrom the Department of Microbiology and Immunology, Nanjing Medical University, Hanzhong Road 140, Nanjing, Jiangsu 210029, China.
Wen QiuFrom the Department of Microbiology and Immunology, Nanjing Medical University, Hanzhong Road 140, Nanjing, Jiangsu 210029, China.
Kai ShanFrom the Department of Microbiology and Immunology, Nanjing Medical University, Hanzhong Road 140, Nanjing, Jiangsu 210029, China.
Jing ZhangFrom the Department of Microbiology and Immunology, Nanjing Medical University, Hanzhong Road 140, Nanjing, Jiangsu 210029, China.
Yanlai LuFrom the Department of Microbiology and Immunology, Nanjing Medical University, Hanzhong Road 140, Nanjing, Jiangsu 210029, China.
Yan LiFrom the Department of Microbiology and Immunology, Nanjing Medical University, Hanzhong Road 140, Nanjing, Jiangsu 210029, China.
Yingwei WangFrom the Department of Microbiology and Immunology, Nanjing Medical University, Hanzhong Road 140, Nanjing, Jiangsu 210029, China wangyw1508@njmu.edu.cn.
Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin 17 (IL-17), produced mainly by T helper 17 (Th17) cells, is increasingly recognized as a key regulator in various autoimmune diseases, including human multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). Although several microRNAs (miRNAs) with aberrant expression have been shown to contribute to the pathogenesis of MS and EAE, the mechanisms underlying the regulation of abnormal miRNA expression in astrocytes upon IL-17 stimulation remain unclear. In the present study, we detected the changes of miRNA expression profiles both in the brain tissue of EAE mice and in cultured mouse primary astrocytes stimulated with IL-17 and identified miR-873 as one of the co-up-regulated miRNAs in vivo and in vitro. The overexpression of miR-873, demonstrated by targeting A20 (TNFα-induced protein 3, TNFAIP3), remarkably reduced the A20 level and promoted NF-κB activation in vivo and in vitro as well as increasing the production of inflammatory cytokines and chemokines (i.e. IL-6, TNF-α, MIP-2, and MCP-1/5). More importantly, silencing the endogenous miR-873 or A20 gene with lentiviral vector of miR-873 sponge (LV-miR-873 sponge) or short hairpin RNA (shRNA) of A20 (LV-A20 shRNA) in vivo significantly lessened or aggravated inflammation and demyelination in the central nervous system (CNS) of EAE mice, respectively. Taken together, these findings indicate that miR-873 induced by IL-17 stimulation promotes the production of inflammatory cytokines and aggravates the pathological process of EAE mice through the A20/NF-κB pathway, which provides a new insight into the mechanism of inflammatory damage in MS.

Indexed as

3' Untranslated RegionsAnimalsAstrocytesCysteine EndopeptidasesDemyelinating DiseasesEncephalomyelitis, Autoimmune, ExperimentalGene Expression RegulationInflammationInterleukin-17Intracellular Signaling Peptides and ProteinsLentivirusMiceMice, Inbred C57BLMicroRNAsNF-kappa BTumor Necrosis Factor alpha-Induced Protein 33' Untranslated RegionsCysteine EndopeptidasesInterleukin-17Intracellular Signaling Peptides and ProteinsMicroRNAsMIRN873 microRNA, mouseNF-kappa BTnfaip3 protein, mouseTumor Necrosis Factor alpha-Induced Protein 3A20AstrocyteCytokineExperimental Autoimmune EncephalomyelitisInterleukin 17A (IL-17 or IL-17A)MicroRNA-873Multiple SclerosisNF-kappaB

Identifiers

PMID25183005
PMCPMC4200254
OpenAlexW2022477030

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.