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Long non‑coding RNA GAS5 protects against Mycoplasma pneumoniae pneumonia by regulating the microRNA‑222‑3p/TIMP3

Likun Yang1, Xifeng Zhang1, Xiufen Liu1

  • 1Pediatric Intensive Care Unit, The Second People's Hospital of Liaocheng, Affiliated to Shandong First Medical University, Linqing, Shandong 252600, P.R. China.

Molecular Medicine Reports
|March 24, 2021
PubMed

Insights

Long non-coding RNA GAS5 enhances cell viability and reduces inflammation in Mycoplasma pneumoniae pneumonia (MPP) by regulating the miR-222-3p/TIMP3 pathway, offering a potential therapeutic target for MPP.

Area of Science:

  • Molecular Biology
  • Immunology
  • Respiratory Medicine

Background:

  • Mycoplasma pneumoniae pneumonia (MPP) is a common respiratory infection.
  • The molecular mechanisms underlying MPP pathogenesis require further elucidation.
  • Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in disease.

Purpose of the Study:

  • To investigate the role of long non-coding RNA growth arrest-specific 5 (GAS5) in MPP.
  • To elucidate the molecular mechanism involving GAS5, microRNA-222-3p (miR-222-3p), and tissue inhibitor of metalloproteinases-3 (TIMP3) in MPP.
  • To assess the therapeutic potential of targeting the GAS5/miR-222-3p/TIMP3 axis in MPP.

Main Methods:

  • Reverse transcription-quantitative PCR (RT-qPCR) to measure gene expression.
  • Lipid-associated membrane protein (LAMP)-induced THP-1 cells as an in vitro MPP model.
  • MTT assay for cell viability assessment.
  • ELISA to quantify pro- and anti-inflammatory cytokines.
  • Dual-luciferase reporter assay to confirm molecular interactions.

Main Results:

  • GAS5 and TIMP3 expression were downregulated, while miR-222-3p was upregulated in MPP.
  • GAS5 overexpression enhanced cell viability and reduced pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) and HO-1 levels in LAMP-induced THP-1 cells.
  • GAS5 directly targeted miR-222-3p, and TIMP3 was a target of miR-222-3p.
  • miR-222-3p upregulation or TIMP3 knockdown reversed the effects of GAS5 overexpression.

Conclusions:

  • GAS5 plays a protective role in MPP by enhancing cell viability and suppressing inflammation.
  • The miR-222-3p/TIMP3 axis mediates the effects of GAS5 in MPP.
  • Targeting the GAS5/miR-222-3p/TIMP3 pathway represents a potential therapeutic strategy for MPP.
Keywords:
Mycoplasma pneumoniae pneumonialong non‑coding RNA GAS5microRNA‑222‑3ptissue inhibitor of metalloproteinases‑3inflammation

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