Long non-coding RNA MEG3 regulates the progress of osteoarthritis by regulating the miR-34a/Klotho axis

Gaoxin Xiong1,2, Shuangli Wang1,2, Zhengjun Pan2

  • 1Department of Bone and Joint Surgery, Institute of Orthopedic Diseases, the First Affiliated Hospital of Jinan University, Jinan University, Guangzhou, China.

Abstract

Insights

Long non-coding RNA MEG3 (lncRNA MEG3) inhibition impacts osteoarthritis progression by regulating the miR-34a/Klotho axis. This study offers new insights into potential therapeutic targets for osteoarthritis treatment.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Genetics

Background:

  • Osteoarthritis (OA) is a prevalent chronic disease with increasing incidence.
  • Understanding the role of long non-coding RNAs (lncRNAs) like maternally expressed gene 3 (MEG3) is crucial for developing novel OA treatments.

Purpose of the Study:

  • To investigate the role of lncRNA MEG3 in osteoarthritis pathogenesis.
  • To explore the potential of targeting lncRNA MEG3 for OA treatment.

Main Methods:

  • Constructed an osteoarthritis mouse model and analyzed knee joint tissues using HE staining and CT.
  • Quantified expression of miR-34a and Klotho via fluorescent quantitative PCR and Western blot.
  • Overexpressed lncRNA MEG3 in C28/I2 cells and assessed changes in target gene and protein expression.

Main Results:

  • Osteoarthritis model mice exhibited significant pathological changes, decreased Klotho, and increased miR-34a expression.
  • Lipopolysaccharide (LPS) treatment led to decreased lncRNA MEG3, Klotho, FGF23, and Bcl-2, with increased miR-34a, Bax, TGF-β1, Caspase 3, and Caspase 8.
  • lncRNA MEG3 overexpression modulated the expression of miR-34a, Klotho, FGF23, Bcl-2, Bax, TGF-β1, Caspase 3, and Caspase 8.

Conclusions:

  • lncRNA MEG3 influences OA progression.
  • The miR-34a/Klotho axis is a key regulatory pathway modulated by lncRNA MEG3 in OA.
  • Targeting lncRNA MEG3 may offer a therapeutic strategy for osteoarthritis.

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