Evidence map›Paper›PMID 23562609›Full record

ArticleThe Journal of allergy and clinical immunology2013

MicroRNA-17/20a/106a modulate macrophage inflammatory responses through targeting signal-regulatory protein α.

Dihan Zhu, Chaoyun Pan, Limin Li, Zhen Bian, Zhiyuan Lv, Lei Shi, Jing Zhang, Donghai Li, Hongwei Gu, Chen-Yu Zhang and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 7% 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

78 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  12. Deciphering the role of CD47 in cancer immunotherapy.Journal of advanced research · 2024
    Review
  13. Article
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  17. Article
  18. Review
  19. Overview of miR-106a Regulatory Roles: from Cancer to Aging.Bioengineering (Basel, Switzerland) · 2023
    Review
  20. Article

18 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

12 authors at 4 institutions in 3 countries.

Dihan ZhuResearch Institute of Nephrology, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China.
Chaoyun Pan
Limin Li
Zhen Bian
Zhiyuan Lv
Lei Shi
Jing Zhang
Donghai Li
Hongwei Gu
Chen-Yu Zhang
Yuan Liu
Ke Zen
Nanjing University · CNGeorgia State University · USNanjing General Hospital of Nanjing Military Command · CNNanjing University of Science and Technology · CN

Funding

Regulating neutrophil response during chronic inflammation through SIRPa alteratiR01AI106839 · NIAID · GEORGIA STATE UNIVERSITY · PI LIU, YUAN · 2014 to 2018
$2.0M
NIAID NIH HHS R01 AI106839
6 · The paper itself

Abstract

backgroundSignal-regulatory protein α (SIRPα) is an essential signaling molecule that modulates leukocyte inflammatory responses. However, the regulation of selective SIRPα synthesis and its dynamic changes in leukocytes under inflammatory stimulation remain incompletely understood.

objectiveWe sought to identify the microRNAs (miRNAs) that posttranscriptionally regulate SIRPα synthesis and their roles in modulating macrophage inflammatory responses.

methodsSIRPα was induced in SIRPα-negative promyelocytic cells by retinoic acid or phorbol 12-myristate 13-acetate, and the differential expression of miRNAs was assessed by means of microarray and quantitative RT-PCR assays. The roles of identified miRNAs in controlling SIRPα synthesis in leukocytes and leukocyte inflammatory responses were determined.

resultsWe identified SIRPα as a common target gene of miR-17, miR-20a, and miR-106a. During SIRPα induction, levels of these 3 miRNAs were all reduced, and their downregulation by retinoic acid or phorbol 12-myristate 13-acetate occurred through suppression of the c-Myc signaling pathway. All miR-17, miR-20a, and miR-106a specifically bound to the same seed sequence within the SIRPα 3' untranslated region and correlated inversely with SIRPα protein levels in various cells. In macrophages upregulation of miR-17, miR-20a, and miR-106a by LPS served as the mechanism underlying LPS-induced SIRPα reduction and macrophage activation. Both in vitro and in vivo assays demonstrate that miR-17, miR-20a, and miR-106a regulate macrophage infiltration, phagocytosis, and proinflammatory cytokine secretion through targeting SIRPα.

conclusionThese findings demonstrate for the first time that miR-17, miR-20a, and miR-106a regulate SIRPα synthesis and SIRPα-mediated macrophage inflammatory responses in a redundant fashion, providing a novel pathway in which a panel of miRNAs can modulate immune polarization through regulation of macrophage activation.

Indexed as

Gene Expression RegulationAnimalsAntigens, DifferentiationCell LineHL-60 CellsHumansInflammationMacrophage ActivationMacrophagesMaleMiceMice, Inbred C57BLMicroRNAsReceptors, ImmunologicSignal TransductionU937 CellsAntigens, DifferentiationMicroRNAsMIRN106 microRNA, humanMIRN17 microRNA, humanMIRN20a microRNA, humanReceptors, ImmunologicSIRPA protein, humanAntisense oligonucleotideASOFITCFluorescein isothiocyanateGalactosylated low-molecular-weight chitosanGAPDHGlyceraldehyde-3-phosphate dehydrogenaseImmunoreceptor tyrosine-based inhibitory motifinflammatory responseITIMmacrophagemicroRNAMicro RNAmiRNAncRNANitric oxideNONormal control RNAPEIPhorbol 12-myristate 13-acetatepre-ncRNAPre-normal control RNARARetinoic acidSignal-regulatory protein αSIRPαSP-ASP-DSurfactant protein ASurfactant protein DTPAUntranslated regionUTR

Identifiers

PMID23562609
PMCPMC5882493
OpenAlexW2070985562

What OpenQuestion holds

Textmetadata
LicenceTDM
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.