Evidence map›Paper›PMID 32792604›Full record

ArticleScientific reports2020

Long non-coding RNA FENDRR regulates IFNγ-induced M1 phenotype in macrophages.

Maria Cristina Munteanu, Chaoqun Huang, Yurong Liang, Roshini Sathiaseelan, Xiangming Zeng, Lin Liu

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 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  8. Role of lncRNAs in pathophysiology of obesity.Current opinion in physiology · 2025
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  15. Long Noncoding RNAInternational journal of molecular sciences · 2021
    Article
  16. Long Non-Coding RNAGenes · 2021
    Review
  17. Article
  18. Article
  19. 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

6 authors at 1 institution in 1 country.

Maria Cristina MunteanuOklahoma Center for Respiratory and Infectious Diseases, Oklahoma State University, Stillwater, OK, USA.
Chaoqun HuangOklahoma Center for Respiratory and Infectious Diseases, Oklahoma State University, Stillwater, OK, USA.
Yurong LiangOklahoma Center for Respiratory and Infectious Diseases, Oklahoma State University, Stillwater, OK, USA.
Roshini SathiaseelanOklahoma Center for Respiratory and Infectious Diseases, Oklahoma State University, Stillwater, OK, USA.
Xiangming ZengOklahoma Center for Respiratory and Infectious Diseases, Oklahoma State University, Stillwater, OK, USA.
Lin LiuOklahoma Center for Respiratory and Infectious Diseases, Oklahoma State University, Stillwater, OK, USA. lin.liu@okstate.edu.ORCID http://orcid.org/0000-0002-4811-4897
Oklahoma State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages play an essential role in host defense and display remarkable plasticity in switching between classically (pro-inflammatory-M1) and alternatively activated (anti-inflammatory-M2) phenotypes. The molecular mechanisms of macrophage polarization are not fully understood. Long non-coding RNAs (lncRNAs) with a length of > 200 nucleotides have been shown to play diverse roles in biological processes. Aberrant expression of lncRNAs is associated with a variety of pathophysiological conditions such as cancer, diabetes, cardiovascular, pulmonary diseases, and tissue fibrosis. In this study, we investigated the role of lncRNA FENDRR in human and mouse macrophage polarization. Human THP-1 monocytes were activated with phorbol-12-myristate-13-acetate (PMA) and differentiated into M1 macrophages with IFNγ or M2 macrophages with IL4. Real-time PCR analysis revealed that FENDRR was expressed 80-fold higher in M1 macrophages than that in M2 macrophages. Overexpression of FENDRR in PMA-activated THP-1 cells increased the IFNγ-induced expression of M1 markers, including IL1β and TNFα at both mRNA and protein levels. Knockdown of FENDRR had an opposite effect. Similarly, FENDRR overexpression in primary mouse bone marrow-derived macrophages increased mRNA expression of M1 markers. FENDRR overexpression increased, while FENDRR knock-down decreased, the IFNγ-induced phosphorylation of STAT1 in PMA-activated THP-1 cells. Our studies suggest that FENDRR enhances IFNγ-induced M1 macrophage polarization via the STAT1 pathway.

Indexed as

Down-RegulationAnimalsCell PolarityGene Knockdown TechniquesHumansInterferon-gammaMacrophage ActivationMiceMonocytesRNA, Long NoncodingSTAT1 Transcription FactorTHP-1 CellsInterferon-gammaRNA, Long NoncodingSTAT1 Transcription Factor

Identifiers

PMID32792604
PMCPMC7426844
OpenAlexW3048750041

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.