Evidence map›Paper›PMID 32665564›Full record

ArticleScientific reports2020

LncRNA RP11-86H7.1 promotes airway inflammation induced by TRAPM2.5 by acting as a ceRNA of miRNA-9-5p to regulate NFKB1 in HBECS.

Jun Zhao, Jinding Pu, Binwei Hao, Lingmei Huang, Jinglong Chen, Wei Hong, Yumin Zhou, Bing Li, Pixin Ran

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.2field-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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
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  3. MicroRNAs as biomarkers and molecular mediators of cognitive dysfunction in schizophrenia.Journal of neural transmission (Vienna, Austria : 1996) · 2026
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  13. The Effects and Pathogenesis of PM2.5 and Its Components on Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2023
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Autophagy Induced by BCL2-Related ceRNA Network Participates in the Occurrence of COPD.International journal of chronic obstructive pulmonary disease · 2022
    Article
  19. Article
  20. Review
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 3 institutions in 1 country.

Jun ZhaoState Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, 195 Dongfeng Xi Road, Guangzhou, 510182, Guangdong, China.
Jinding PuState Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, 195 Dongfeng Xi Road, Guangzhou, 510182, Guangdong, China.
Binwei HaoState Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, 195 Dongfeng Xi Road, Guangzhou, 510182, Guangdong, China.
Lingmei HuangState Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, 195 Dongfeng Xi Road, Guangzhou, 510182, Guangdong, China.
Jinglong ChenState Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, 195 Dongfeng Xi Road, Guangzhou, 510182, Guangdong, China.
Wei HongState Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, 195 Dongfeng Xi Road, Guangzhou, 510182, Guangdong, China.
Yumin ZhouState Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, 195 Dongfeng Xi Road, Guangzhou, 510182, Guangdong, China.
Bing LiGMU-GIBH Joint School of Life Sciences, Guangzhou Medical University, Guangzhou, Guangdong, China.
Pixin RanState Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, 195 Dongfeng Xi Road, Guangzhou, 510182, Guangdong, China. pxran@gzhmu.edu.cn.
First Affiliated Hospital of Guangzhou Medical University · CNGuangzhou Medical University · CNState Key Laboratory of Respiratory Disease · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traffic-related air pollution particulate matter 2.5 (TRAPM2.5), is involved in chronic obstructive pulmonary disease (COPD), which is characterized by airway inflammation. Specifically, these harmful particles or gases can increase chronic airway inflammation. Some recent studies have shown that lncRNAs are closely related to COPD and participate in the regulation of airway inflammation. However, the precise mechanisms remain unknown. In the present study, we investigated the effect of TRAPM2.5 on airway inflammation in human bronchial epithelial cells (HBECs) and the underlying mechanisms mediated by a lncRNA. After exposure to TRAPM2.5, the novel lncRNA RP11-86H7.1 was markedly upregulated in HBECs. Functional assays indicated that the lncRNA RP11-86H7.1 was required for the TRAPM2.5-induced expression of inflammatory factors in HBECs. A mechanistic study demonstrated that lncRNA RP11-86H7.1 might participate in TRAPM2.5-induced inflammatory responses by activating the NF-κB signaling pathway. Moreover, the lncRNA RP11-86H7.1 can promote the inflammatory response by acting as a competing endogenous RNA of miR-9-5p, reversing the inhibitory effect of its target gene NFKB1, and sustaining NF-κB activation. In summary, our study elucidates the pro-inflammatory roles of the lncRNA RP11-86H7.1-miR-9-5p-NFKB1 regulatory network in airway inflammation induced by TRAPM2.5 and indicates that the components of this network might serve as novel diagnostic biomarkers and potential therapeutic targets.

Indexed as

BronchiEpithelial CellsGene Expression RegulationHumansInflammationLungMicroRNAsNF-kappa B p50 SubunitParticulate MatterPulmonary Disease, Chronic ObstructiveRNA, Long NoncodingVehicle EmissionsMicroRNAsMIRN92 microRNA, humanNF-kappa B p50 SubunitNFKB1 protein, humanParticulate MatterRNA, Long NoncodingVehicle Emissions

Identifiers

PMID32665564
PMCPMC7360621
OpenAlexW3043372178

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.