Evidence map›Paper›PMID 31949658›Full record

ArticleInternational journal of clinical and experimental pathology2018

MicroRNA-182-5p inhibits inflammation in LPS-treated RAW264.7 cells by mediating the TLR4/NF-κB signaling pathway.

Minjie Zhu, Yang Li, Keyu Sun

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

10 citing papers in PubMed, 12 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 1 institution in 1 country.

Minjie ZhuDepartment of Emergency, Minhang Branch of Zhongshan Hospital, Fudan University Shanghai, China.
Yang LiDepartment of Emergency, Minhang Branch of Zhongshan Hospital, Fudan University Shanghai, China.
Keyu SunDepartment of Emergency, Minhang Branch of Zhongshan Hospital, Fudan University Shanghai, China.
Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive inflammation is predominantly involved in the pathogenesis of acute lung injury (ALI). Recently, microRNAs (miRNAs) have been shown to act as an important regulator of inflammation. Hence, we investigated the levels of miR-182-5p and its functional role about regulating inflammation in LPS-induced ALI mice and RAW264.7 cells. Here, LPS induced-ALI model was established in male mice. By qRT-PCR, we found that the expression of miR-182-5p was significantly downregulated in lung tissue and bronchoalveolar lavage fluid (BALF), as well as decreased in LPS-treated RAW264.7 cells. In vitro, overexpression of miR-182-5p suppressed the inflammatory response, as evidenced by reduction of pro-inflammatory cytokines including interleukin (IL)-6, IL-1β, and tumor necrosis factor-α (TNF-α). Further experiments revealed that toll-like receptor 4 (TLR4) was the target of miR-182-5p, which was confirmed by luciferase activity assay. Moreover, RAW264.7 cells transfected with pcDNA-TLR4 plasmid abrogated the protective effects of miR-182-5p against LPS-induced inflammatory response. Additionally, we observed that overexpression of miR-182-5p blocked LPS-induced activation of the NF-κB signaling pathway by targeting TLR4. Collectively, the findings of our study indicate that miR-182-5p inhibits the inflammatory response by modulating TLR4/NF-κB signaling pathway in LPS-treated RAW264.7 cells.

Indexed as

Acute lung injuryinflammatory responseMicroRNA-182-5pTLR4/NF-κB signaling pathway

Identifiers

PMID31949658
PMCPMC6963093
OpenAlexW3006604081

What OpenQuestion holds

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Registered trials

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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.