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Abnormal Expression of DICER1 Leads to Dysregulation of Inflammatory Effectors in Human Synoviocytes

Congshan Jiang1,2, Jing Xu1,2, Wenhua Zhu1,2

  • 1Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, No. 76 Yanta West Road, Xi'an, Shaanxi, China.

Mediators of Inflammation
|July 6, 2019
PubMed

Insights

DICER1 deficiency promotes rheumatoid arthritis (RA) inflammation by increasing pro-inflammatory factors and reducing apoptosis in synoviocytes. Restoring DICER1 levels may offer a therapeutic target for RA.

Area of Science:

  • Molecular Biology
  • Immunology
  • Rheumatology

Background:

  • MicroRNA (miRNA) dysregulation is common in rheumatoid arthritis (RA).
  • The role of DICER1, crucial for miRNA biogenesis, in RA pathogenesis remains unclear.

Purpose of the Study:

  • To investigate the mechanism of DICER1 deficiency-induced inflammation in human SW982 synoviocytes.
  • To explore DICER1's role in regulating RA-related miRNAs and cellular processes.

Main Methods:

  • RNA interference (RNAi) and overexpression of DICER1 in SW982 cells.
  • Analysis of protein production (COX2, MMPs, TGF-β1, TIMP1) and cytokine levels (IL-8).
  • Assessment of apoptosis and proliferation, miRNA expression profiling, and Ingenuity Pathway Analysis (IPA).

Main Results:

  • DICER1 deficiency increased pro-inflammatory mediators (COX2, MMP3, MMP13, IL-8) and decreased anti-inflammatory factors (TGF-β1, TIMP1).
  • DICER1 deficiency reduced apoptosis and increased proliferation, while DICER1 overexpression reversed these effects.
  • DICER1 deficiency lowered RA-related miRNA expression (e.g., miR-155), which in turn regulated MMP3 and MMP13 levels.

Conclusions:

  • DICER1 deficiency drives pro-inflammatory events and aberrant cell behavior in synoviocytes, contributing to RA pathogenesis.
  • DICER1 regulates RA-related miRNAs, suggesting its downstream targets mediate inflammatory destruction and proliferation.
  • Targeting DICER1 or its miRNA pathways presents a potential therapeutic strategy for rheumatoid arthritis.

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