Evidence map›Paper›PMID 31660971›Full record

ArticleRespiratory research2019

Down-regulation of long non-coding RNA SNHG14 protects against acute lung injury induced by lipopolysaccharide through microRNA-34c-3p-dependent inhibition of WISP1.

Jinyuan Zhu, Jijia Bai, Shaojin Wang, Hui Dong

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 37 citations in OpenAlex.

  1. LncRNA SNHG14 drives alveolar inflammation in bronchopulmonary dysplasia via DNMT3a-mediated epigenetic silencing of miR-214-3p.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  20. Knockdown of SNHG14 Alleviates MPPFrontiers in neuroscience · 2020
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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

4 authors at 2 institutions in 1 country.

Jinyuan ZhuDepartment of Critical Care Medicine, General Hospital of Ningxia Medical University, Yinchuan, 750004, People's Republic of China.
Jijia BaiDepartment of Critical Care Medicine, General Hospital of Ningxia Medical University, Yinchuan, 750004, People's Republic of China.
Shaojin WangDepartment of Respiratory and Critical Care Medicine, General Hospital of Ningxia Medical University, Yinchuan, 750004, People's Republic of China.
Hui DongCenter of Research Equipment Management, General Hospital of Ningxia Medical University, No. 804, Shengli South Street, Xingqing District, Yinchuan, 750004, Ningxia Hui Autonomous Region, People's Republic of China. 173401951@qq.com.
Ningxia Medical University · CNNingxia Medical University General Hospital · CN

Funding

NingXia Natural Science Foundation of China 2019AAC03182the Plan of Talented Personnel Project for Youth in Ningxia Autonomous Region (2017) None
6 · The paper itself

Abstract

backgroundAccumulating evidence has shown the important roles of long non-coding RNAs (lncRNAs) in acute lung injury (ALI). This study aimed to investigate the potential role of lncRNA small nucleolar RNA host gene 14 (SNHG14) in lipopolysaccharides (LPS)-induced ALI.

methodsExpression of SNHG14, microRNA-34c-3p (miR-34c-3p) and Wnt1 inducible signaling pathway protein 1 (WISP1) in LPS-exposed mouse alveolar macrophages (MH-S) and lung tissues from mice with LPS-induced ALI was determined by reverse transcription quantitative polymerase chain reaction. The interactions among SNHG14, miR-34c-3p and WISP1 were analyzed by dual-luciferase reporter and RIP assays. Using gain-of-function or loss-of-function approaches, the contents of proinflammatory proteins were determined and MH-S cell viability was assessed to evaluate the in vitro functions of SNHG14, miR-34c-3p and WISP1, and wet/dry weight ratio and proinflammatory proteins in lung tissues were determined to assess their in vivo effects.

resultsSNHG14 and WISP1 expression was increased, while miR-34c-3p was decreased in ALI models. SNHG14 bound to miR-34c-3p, resulting in impaired miR-34c-3p-dependent down-regulation of WISP1. Both SNHG14 silencing and miR-34c-3p over-expression reduced the levels of proinflammatory proteins IL-18, IL-1β, TNF-α and IL-6 and inhibited MH-S cell viability. SNHG14 silencing or miR-34c-3p over-expression decreased the wet/dry weight ratio in lung tissues from ALI mice. The reductions induced by SNHG14 silencing or miR-34c-3p over-expression were rescued by WISP1 over-expression.

conclusionThis study demonstrated that lncRNA SNHG14 silencing alleviated inflammation in LPS-induced ALI through miR-34c-3p-mediated inhibition of WISP1. Our findings suggest that lncRNA SNHG14 may serve as a therapeutic target for ALI.

Indexed as

Acute Lung InjuryAnimalsCCN Intercellular Signaling ProteinsCells, CulturedDown-RegulationLipopolysaccharidesMacrophages, AlveolarMiceMice, Inbred BALB CMice, Inbred ICRMicroRNAsProto-Oncogene ProteinsRandom AllocationRNA, Long NoncodingCCN4 protein, mouseCCN Intercellular Signaling ProteinsLipopolysaccharidesMicroRNAsMIRN34a microRNA, mouseProto-Oncogene ProteinsRNA, Long NoncodingAcute lung injuryLipopolysaccharideLong non-coding RNA SNHG14MicroRNA-34c-3pWnt1 inducible signaling pathway protein 1

Identifiers

PMID31660971
PMCPMC6819549
OpenAlexW2981898992

What OpenQuestion holds

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LicenceCC BY
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.