Evidence map›Paper›PMID 30231673›Full record

ArticleCell cycle (Georgetown, Tex.)2018

MicroRNA-27a alleviates LPS-induced acute lung injury in mice via inhibiting inflammation and apoptosis through modulating TLR4/MyD88/NF-κB pathway.

MinJie Ju, BoFei Liu, HongYu He, ZhunYong Gu, YiMei Liu, Ying Su, DuMing Zhu, Jing Cang, Zhe Luo

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed
6.2field-weighted citation impact, top 2% 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

117 citing papers in PubMed, 238 citations in OpenAlex.

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  10. Network pharmacology approach to unveiling the mechanism of berberine in the amelioration of morphine tolerance.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025
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  19. Dexamethasone relieves the inflammatory response caused by inguinal hernia meshes through miR-155.Hernia : the journal of hernias and abdominal wall surgery · 2024
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57 more citing papers are in PubMed but not listed here.

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

9 authors at 4 institutions in 1 country.

MinJie Jua Department of Critial Care Medicine , Zhongshan Hospital, Fudan University , Shanghai China.
BoFei Liub Department of Intensive Care Medicine , 1st People Hospital , ZhangjiaGang , China.
HongYu Hea Department of Critial Care Medicine , Zhongshan Hospital, Fudan University , Shanghai China.
ZhunYong Gua Department of Critial Care Medicine , Zhongshan Hospital, Fudan University , Shanghai China.
YiMei Liua Department of Critial Care Medicine , Zhongshan Hospital, Fudan University , Shanghai China.
Ying Sua Department of Critial Care Medicine , Zhongshan Hospital, Fudan University , Shanghai China.
DuMing Zhua Department of Critial Care Medicine , Zhongshan Hospital, Fudan University , Shanghai China.
Jing Cangc Department of Anesthesiology , Zhongshan Hospital, Fudan University , Shanghai , China.
Zhe Luoa Department of Critial Care Medicine , Zhongshan Hospital, Fudan University , Shanghai China.
Zhongshan Hospital · CNFudan University · CNThe First Affiliated Hospital, Sun Yat-sen University · CNZhangjiagang First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute lung injury (ALI) is a critical clinical condition with a high mortality rate, characterized with excessive uncontrolled inflammation and apoptosis. Recently, microRNAs (miRNAs) have been found to play crucial roles in the amelioration of various inflammation-induced diseases, including ALI. However, it remains unknown the biological function and regulatory mechanisms of miRNAs in the regulation of inflammation and apoptosis in ALI. The aim of this study is to identify and evaluate the potential role of miRNAs in ALI and reveal the underlying molecular mechanisms of their effects. Here, we analyzed microRNA expression profiles in lung tissues from LPS-challenged mice using miRNA microarray. Because microRNA-27a (miR-27a) was one of the miRNAs being most significantly downregulated, which has an important role in regulation of inflammation, we investigated its function. Overexpression of miR-27a by agomir-27a improved lung injury, as evidenced by the reduced histopathological changes, lung wet/dry (W/D) ratio, lung microvascular permeability and apoptosis in the lung tissues, as well as ameliorative survival of ALI mice. This was accompanied by the alleviating of inflammation, such as the reduced total BALF cell and neutrophil counts, decreased levels of tumor necrosis factor alpha (TNF-α), interleukin-1 (IL-6) interleukin-1β (IL-1β) and myeloperoxidase (MPO) activity in BAL fluid. Toll-like receptor 4 (TLR4), an important regulator of the nuclear factor kappa-B (NF-κB) signaling pathway, was identified as a novel target of miR-27a in RAW264.7 cells. Furthermore, our results showed that LPS stimulation increased the expression of MyD88 and NF-κB p65 (p-p65), but inhibited the expression of inhibitor of nuclear factor-κB-α (IκB-α), suggesting the activation of NF-κB signaling pathway. Further investigations revealed that agomir-miR-27a reversed the promoting effect of LPS on NF-κB signaling pathway. The results here suggested that miR-27a alleviates LPS-induced ALI in mice via reducing inflammation and apoptosis through blocking TLR4/MyD88/NF-κB activation.

Indexed as

ApoptosisAcute Lung InjuryAnimalsBase SequenceDown-RegulationInflammationLipopolysaccharidesMiceMice, Inbred BALB CMicroRNAsModels, BiologicalMyeloid Differentiation Factor 88NF-kappa BRAW 264.7 CellsSignal TransductionToll-Like Receptor 4LipopolysaccharidesMicroRNAsMirn27 microRNA, mouseMyeloid Differentiation Factor 88NF-kappa BToll-Like Receptor 4Acute lung injuryinflammation and apoptosismicroRNA-27aTLR4/MyD88/NF-κB pathway

Identifiers

PMID30231673
PMCPMC6260216
OpenAlexW2891237012

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.