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Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
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RelA/MicroRNA-30a/NLRP3 signal axis is involved in rheumatoid arthritis via regulating NLRP3 inflammasome in

Qiudong Yang1,2,3,4, Wenhua Zhao1,3,4, Yuyi Chen2,3,4

  • 1Department of Basic Science of Stomatology, The Affiliated Stomatological Hospital of Nanjing Medical University, Nanjing, China.

Cell Death & Disease
|November 9, 2021
PubMed

Insights

The RelA/miR-30a/NLRP3 signaling axis regulates the NLRP3 inflammasome in rheumatoid arthritis (RA) macrophages. Targeting this axis with miR-30a can reduce joint inflammation and bone damage in RA.

Area of Science:

  • Immunology
  • Molecular Biology
  • Rheumatology

Background:

  • The NLRP3 inflammasome is implicated in rheumatoid arthritis (RA) pathogenesis.
  • Post-transcriptional regulation of NLRP3 by microRNAs (miRNAs) in synovial macrophages remains poorly understood.

Purpose of the Study:

  • To investigate the role of miRNA-mediated post-transcriptional regulation of the NLRP3 inflammasome in RA.
  • To elucidate the mechanisms underlying RA pathogenesis involving the RelA/miR-30a/NLRP3 signaling axis.

Main Methods:

  • Utilized NLRP3-deficient (NLRP3KO) and TNFα-transgenic (TNFTG) mice (NLRP3KO/TNFTG) to study joint phenotypes.
  • Analyzed synovial macrophage markers (F4/80+, Caspase-1+, IL-1β+) and bone parameters (osteoblasts, osteoclasts).
  • Investigated the regulatory relationship between RelA, miR-30a, and NLRP3 in bone marrow-derived macrophages (BMDMs) and therapeutic potential of AAV-miR-30a in vivo.

Main Results:

  • TNFTG mice exhibited increased joint inflammation and bone erosion compared to wild-type (WT) mice.
  • NLRP3 knockout ameliorated joint inflammation and bone damage in TNFTG mice.
  • RelA positively regulated NLRP3 but negatively regulated miR-30a; miR-30a directly targeted NLRP3, forming a feedforward loop. Intra-articular AAV-miR-30a injection reduced RA phenotypes in TNFTG mice.

Conclusions:

  • The RelA/miR-30a/NLRP3 signaling axis is a key regulator of the NLRP3 inflammasome in RA pathogenesis.
  • Targeting this axis, specifically with miR-30a, demonstrates therapeutic potential for reducing joint inflammation and bone damage in RA.

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