Evidence map›Paper›PMID 26971344›Full record

ArticleCellular and molecular neurobiology2017

MicroRNA-27a Negatively Modulates the Inflammatory Response in Lipopolysaccharide-Stimulated Microglia by Targeting TLR4 and IRAK4.

Yan-Ni Lv, Ai-Jun Ou-Yang, Long-Sheng Fu

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

Article in Cellular and molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

49 citing papers in PubMed, 67 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

3 authors at 2 institutions in 1 country.

Yan-Ni LvPharmacy Department, The First Affiliated Hospital of Nanchang University, Yongwai Street 17, Nanchang, 330006, People's Republic of China. lvyanni@126.com.
Ai-Jun Ou-YangPharmacy Department, The First Affiliated Hospital of Nanchang University, Yongwai Street 17, Nanchang, 330006, People's Republic of China.
Long-Sheng FuPharmacy Department, The First Affiliated Hospital of Nanchang University, Yongwai Street 17, Nanchang, 330006, People's Republic of China.
Nanchang University · CNFirst Affiliated Hospital of Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

microRNA, a family of small non-coding RNA, plays significant roles in regulating gene expression, mainly via binding to the 3'-untranslated region of target genes. Although the role of miRNA in regulating neuroinflammation via the innate immune pathway has been studied, its role in the production of inflammatory mediators during microglial activation is poorly understood. In this study, we investigated the effect of miR-27a on lipopolysaccharide (LPS)-induced microglial inflammation. miR-27a expression was found to be rapidly decreased in microglia by real-time polymerase chain reaction (real-time PCR) after LPS stimulation. Over-expression of miR-27a significantly decreased the production of inflammatory cytokines, such as interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and nitric oxide (NO), whereas knockdown of miR-27a increased the expression of these inflammatory factors. We also demonstrated by loss- and gain-of-function studies that miR-27a directly suppressed the expression of toll-like receptor 4 (TLR4) and interleukin-1 receptor-associated kinase 4 (IRAK4)-a pivotal adaptor kinase in the TLR4/MyD88 signaling pathway-by directly binding their 3'-UTRs: knocking down TLR4 or IRAK4 in microglia significantly decreased TLR4 or IRAK4 expression and inhibited the downstream production of inflammatory mediators. Moreover, the inflammatory cytokines IL-6 and IL-1β were regulated by IRAK4, whereas TNF-α and NO were more dependent on TLR4 activation. Thus, miR-27a might regulate the LPS-induced production of inflammatory cytokines in microglia independently of TLR4 and IRAK4. Taken together, our results suggest that miR-27a is associated with microglial activation and the inflammatory response.

Indexed as

AnimalsAnimals, NewbornCells, CulturedDose-Response Relationship, DrugFemaleGene TargetingInflammation MediatorsLipopolysaccharidesMicrogliaMicroRNAsMolecular MimicryProtein Serine-Threonine KinasesRatsRats, Sprague-DawleyToll-Like Receptor 4Inflammation MediatorsIRAK4 protein, ratLipopolysaccharidesMicroRNAsMirn27 microRNA, mouseProtein Serine-Threonine KinasesTlr4 protein, ratToll-Like Receptor 4IRAK4LipopolysaccharideMicrogliamicroRNANeuroinflammationTLR4

Identifiers

PMID26971344
PMCPMC11482108
OpenAlexW2293543854

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.