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METTL3-mediated m

Yuting Tang1, Fangling Hong1, Siyang Ding2

  • 1Department of Medical Genetics, Nanjing Medical University, Longmian Road 101, Nanjing 211166, P.R. China; Jiangsu Key Laboratory of Xenotransplantation, Nanjing Medical University, Longmian Road 101, Nanjing 211166, P.R. China.

Cell Reports
|June 4, 2023
PubMed
Summary
This summary is machine-generated.

Long noncoding RNA IGFBP7-OT promotes osteoarthritis (OA) by increasing IGFBP7 expression and cartilage degeneration. Its N6-methyladenosine modification offers a potential therapeutic target for OA treatment.

Keywords:
CP: ImmunologyDNA methylationIGFBP7IGFBP7-OTMETTL3osteoarthritis

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Genetics

Background:

  • Osteoarthritis (OA) is a prevalent degenerative joint disease impacting the elderly.
  • Long noncoding RNAs (lncRNAs) are increasingly recognized for their roles in disease pathogenesis.

Purpose of the Study:

  • To investigate the role of lncRNA IGFBP7-OT in osteoarthritis.
  • To elucidate the molecular mechanisms underlying IGFBP7-OT's function in OA.

Main Methods:

  • Analysis of IGFBP7-OT and IGFBP7 expression in osteoarthritic cartilage.
  • In vitro studies on chondrocyte viability, apoptosis, and extracellular matrix.
  • In vivo assessment of OA phenotype using a mouse model.
  • Mechanistic studies involving DNA methylation and m6A modification.

Main Results:

  • IGFBP7-OT and IGFBP7 are upregulated and positively correlated in OA cartilage.
  • IGFBP7-OT overexpression inhibits chondrocyte viability, promotes apoptosis, and reduces extracellular matrix.
  • IGFBP7-OT knockdown yields opposite effects, ameliorating OA phenotypes.
  • IGFBP7-OT promotes OA by upregulating IGFBP7 via suppression of DNMT1/DNMT3a methylation.
  • METTL3-mediated m6A modification partially controls IGFBP7-OT upregulation in OA.

Conclusions:

  • IGFBP7-OT promotes OA progression through the DNMT1/DNMT3a-IGFBP7 axis.
  • METTL3-mediated m6A modification of IGFBP7-OT is involved in OA pathogenesis.
  • IGFBP7-OT represents a potential therapeutic target for osteoarthritis.