Evidence map›Paper›PMID 32825525›Full record

ArticleGenes2020

Inhibition of miRNA-34a Promotes M2 Macrophage Polarization and Improves LPS-Induced Lung Injury by Targeting Klf4.

Mohd Junaid Khan, Prithvi Singh, Ravins Dohare, Rishabh Jha, Arshad H Rahmani, Saleh A Almatroodi, Shakir Ali, Mansoor Ali Syed

Open access · goldAbstract read
In one paragraph

Article in Genes, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 2 pooled it
1.8field-weighted citation impact, top 15% 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, 2 syntheses or guidelines pooled it, 38 citations in OpenAlex.

  1. miRNAs Related to Immune Checkpoint Inhibitor Response: A Systematic Review.International journal of molecular sciences · 2024
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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

8 authors at 4 institutions in 2 countries.

Mohd Junaid KhanTranslational Research Lab, Department of Biotechnology, Faculty of Natural Sciences, Jamia Millia Islamia, New Delhi 110025, India.
Prithvi SinghCentre for Interdisciplinary Research in Basic Sciences, Jamia Millia Islamia, New Delhi 110025, India.ORCID 0000-0002-2562-0914
Ravins DohareCentre for Interdisciplinary Research in Basic Sciences, Jamia Millia Islamia, New Delhi 110025, India.ORCID 0000-0002-0602-3719
Rishabh JhaCentre for Interdisciplinary Research in Basic Sciences, Jamia Millia Islamia, New Delhi 110025, India.
Arshad H RahmaniDepartment of Medical Laboratories, College of Applied Medical Sciences, Qassim University, Buraydah 51452, Saudi Arabia.
Saleh A AlmatroodiDepartment of Medical Laboratories, College of Applied Medical Sciences, Qassim University, Buraydah 51452, Saudi Arabia.
Shakir AliDepartment of Biochemistry, School of Chemical and Life Sciences Jamia Hamdard, New Delhi 110025, India.ORCID 0000-0002-4002-1231
Mansoor Ali SyedTranslational Research Lab, Department of Biotechnology, Faculty of Natural Sciences, Jamia Millia Islamia, New Delhi 110025, India.ORCID 0000-0003-2697-7832
Jamia Millia Islamia · INDepartment of Biotechnology · INQassim University · SAJamia Hamdard · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute respiratory distress syndrome (ARDS) is an outcome of an accelerated immune response that starts initially as a defensive measure, however, due to non-canonical signaling, it later proves to be fatal not only to the affected tissue but to the whole organ system. microRNAs are known for playing a decisive role in regulating the expression of genes involved in diverse functions such as lung development, repair, and inflammation. In-silico analyses of clinical data and microRNA databases predicted a probable interaction between miRNA-34a (miR-34a), mitogen-activated protein kinase 1 (ERK), and kruppel like factor 4 (Klf4). Parallel to in silico results, here, we show that intra-tracheal instillation of lipopolysaccharides (LPS) to mice enhanced miR-34a expression in lung macrophages. Inhibition of miR-34a significantly improved lung histology, whereas over-expression of miR-34a worsened the lung injury phenotype. miR-34a over-expression in macrophages were also demonstrated to favour pro-inflammatory M1 phenotype and inhibition of M2 polarization. In a quest to confirm this likely interaction, expression profiles of Klf4 as the putative target were analyzed in different macrophage polarizing conditions. Klf4 expression was found to be prominent in the miR-34a inhibitor-treated group but down-regulated in the miR-34a mimic treated group. Immuno-histopathological analyses of lung tissue from the mice treated with miR-34a inhibitor also showed reduced inflammatory M1 markers as well as enhanced cell proliferation. The present study indicates that miR-34a intensified LPS-induced lung injury and inflammation by regulating Klf4 and macrophage polarization, which may serve as a potential therapeutic target for acute lung injury/ARDS.

Indexed as

AnimalsFemaleGene Expression RegulationKruppel-Like Factor 4Kruppel-Like Transcription FactorsLipopolysaccharidesLung InjuryMacrophagesMaleMiceMice, Inbred C57BLMicroRNAsSignal TransductionKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsLipopolysaccharidesMicroRNAsMIRN34a microRNA, mouseacute lung injuryinnate immunitymacrophage subsetsmicroRNAs

Identifiers

PMID32825525
PMCPMC7563942
OpenAlexW3071603197

What OpenQuestion holds

Textmetadata
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.