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Updated: Dec 12, 2025

Using RNA-interference to Investigate the Innate Immune Response in Mouse Macrophages
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Long non-coding RNA FENDRR regulates IFNγ-induced M1 phenotype in macrophages

Maria Cristina Munteanu1,2, Chaoqun Huang1,2, Yurong Liang1,2

  • 1Oklahoma Center for Respiratory and Infectious Diseases, Oklahoma State University, Stillwater, OK, USA.

Scientific Reports
|August 15, 2020
PubMed

Insights

Long non-coding RNA FENDRR promotes M1 macrophage polarization. This study shows FENDRR enhances pro-inflammatory responses via the STAT1 pathway, offering insights into macrophage function.

Area of Science:

  • Immunology
  • Molecular Biology
  • Epigenetics

Background:

  • Macrophages are crucial for host defense, with plasticity to adopt M1 (pro-inflammatory) or M2 (anti-inflammatory) phenotypes.
  • The molecular regulation of macrophage polarization remains incompletely understood.
  • Long non-coding RNAs (lncRNAs) are implicated in various diseases and biological processes.

Purpose of the Study:

  • To investigate the role of lncRNA FENDRR in human and mouse macrophage polarization.
  • To elucidate the molecular mechanisms by which FENDRR influences M1 macrophage activation.

Main Methods:

  • Human THP-1 monocytes and primary mouse bone marrow-derived macrophages were used.
  • Macrophage polarization was induced using phorbol-12-myristate-13-acetate (PMA), IFNγ (for M1), and IL4 (for M2).
  • Real-time PCR, Western blotting, and FENDRR overexpression/knockdown techniques were employed.

Main Results:

  • FENDRR expression was significantly higher (80-fold) in M1 macrophages compared to M2 macrophages.
  • FENDRR overexpression enhanced IFNγ-induced M1 markers (IL1β, TNFα) at mRNA and protein levels.
  • FENDRR modulated IFNγ-induced STAT1 phosphorylation, suggesting involvement in the STAT1 signaling pathway.

Conclusions:

  • FENDRR promotes M1 macrophage polarization.
  • FENDRR enhances IFNγ-induced M1 macrophage activation, potentially through the STAT1 signaling pathway.
  • FENDRR represents a novel regulator of macrophage polarization with implications for inflammatory diseases.

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