Evidence map›Paper›PMID 27498764›Full record

ArticleScientific reports2016

Regulation of proinflammatory genes by the circulating microRNA hsa-miR-939.

Marguerite K McDonald, Sujay Ramanathan, Andrew Touati, Yiqian Zhou, Rushi U Thanawala, Guillermo M Alexander, Ahmet Sacan, Seena K Ajit

Abstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Review
  6. MicroRNA-939 amplifiesFrontiers in immunology · 2024
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. [Complex regional pain syndrome-An update].Schmerz (Berlin, Germany) · 2022
    Article
  13. Article
  14. Hsa-miR-605 regulates the proinflammatory chemokine CXCL5 in complex regional pain syndrome.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
    Article
  15. Article
  16. Article
  17. Non-coding RNAs in neuropathic pain.Neuronal signaling · 2020
    Review
  18. Article
  19. Review
  20. Article
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.

Marguerite K McDonaldPharmacology &Physiology, Drexel University College of Medicine, 245 North 15th Street, Philadelphia, PA 19102, USA.
Sujay RamanathanPharmacology &Physiology, Drexel University College of Medicine, 245 North 15th Street, Philadelphia, PA 19102, USA.
Andrew TouatiPharmacology &Physiology, Drexel University College of Medicine, 245 North 15th Street, Philadelphia, PA 19102, USA.
Yiqian ZhouSchool of Biomedical Engineering, Science &Health Systems, Drexel University, 3141 Chestnut Street, Philadelphia, PA 19104, USA.
Rushi U ThanawalaPharmacology &Physiology, Drexel University College of Medicine, 245 North 15th Street, Philadelphia, PA 19102, USA.
Guillermo M AlexanderNeurology, Drexel University College of Medicine, 245 North 15th Street, Philadelphia, PA 19102, USA.
Ahmet SacanSchool of Biomedical Engineering, Science &Health Systems, Drexel University, 3141 Chestnut Street, Philadelphia, PA 19104, USA.
Seena K AjitPharmacology &Physiology, Drexel University College of Medicine, 245 North 15th Street, Philadelphia, PA 19102, USA.

Funding

Functional characterization of hsa-mir-939 as a novel regulator of painR21NS082991 · NINDS · DREXEL UNIVERSITY · PI AJIT, SEENA · 2013 to 2014
$423k
NINDS NIH HHS R21 NS082991
6 · The paper itself

Abstract

Circulating microRNAs are beneficial biomarkers because of their stability and dysregulation in diseases. Here we sought to determine the role of miR-939, a miRNA downregulated in patients with complex regional pain syndrome (CRPS). Hsa-miR-939 is predicted to target several proinflammatory genes, including IL-6, VEGFA, TNFα, NFκB2, and nitric oxide synthase 2 (NOS2A). Binding of miR-939 to the 3' untranslated region of these genes was confirmed by reporter assay. Overexpression of miR-939 in vitro resulted in reduction of IL-6, NOS2A and NFκB2 mRNAs, IL-6, VEGFA, and NOS2 proteins and NFκB activation. We observed a significant decrease in the NOS substrate l-arginine in plasma from CRPS patients, suggesting reduced miR-939 levels may contribute to an increase in endogenous NOS2A levels and NO, and thereby to pain and inflammation. Pathway analysis showed that miR-939 represents a critical regulatory node in a network of inflammatory mediators. Collectively, our data suggest that miR-939 may regulate multiple proinflammatory genes and that downregulation of miR-939 in CRPS patients may increase expression of these genes, resulting in amplification of the inflammatory pain signal transduction cascade. Circulating miRNAs may function as crucial signaling nodes, and small changes in miRNA levels may influence target gene expression and thus disease.

Indexed as

Gene Expression RegulationCells, CulturedCirculating MicroRNAComplex Regional Pain SyndromesGene Expression ProfilingHumansImmunologic FactorsInflammationMicroRNAsCirculating MicroRNAImmunologic FactorsMicroRNAsMIRN939 microRNA, human

Identifiers

PMID27498764
PMCPMC4976376

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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.