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Over-expression of microRNA-145 Elevating Autophagy Activities via Downregulating FRS2 Expression

Ke Tian1, Bin Deng2, Xiaodong Han2

  • 1Department of Orthopedics and Joint, Affiiated Hospital of Jining Medical University, Shandong, 272001, China.

Combinatorial Chemistry & High Throughput Screening
|June 2, 2023
PubMed
Abstract

Insights

MicroRNA-145 (miR-145) protects chondrocytes in osteoarthritis (OA) by regulating autophagy. Lower miR-145 levels in OA may indicate early disease and offer a therapeutic target.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Osteoarthritis (OA) is a prevalent degenerative joint disease causing cartilage breakdown and chondrocyte death.
  • MicroRNA-145 (miR-145) is known to modulate autophagy in various cell types, but its role in OA chondrocytes remains unexplored.

Purpose of the Study:

  • To investigate the role of miR-145 in regulating chondrocyte autophagy during osteoarthritis development.
  • To determine if miR-145 expression levels correlate with OA progression and chondrocyte viability.

Main Methods:

  • Analysis of miR-145 expression in human OA joint samples.
  • Dual luciferase assay to confirm the targeting relationship between miR-145 and FRS2.
  • Assessment of chondrocyte autophagy and viability following manipulation of miR-145 and FRS2 levels.

Main Results:

  • miR-145 expression and autophagy markers (LC3-II/LC3-I ratio) were decreased, while SQSTM1 expression was increased in OA patients.
  • Overexpression of miR-145 in chondrocytes enhanced autophagy, increased cell viability under oxidative stress, and reduced SQSTM1 levels.
  • FRS2 was identified as a direct target of miR-145, mediating its suppressive effect on autophagy via the PI3K/Akt/mTOR pathway.

Conclusions:

  • miR-145 functions as a protective factor in chondrocytes by regulating the miR-145/FRS2/autophagy axis.
  • Decreased miR-145 in synovial fluid could serve as an early diagnostic marker for OA.
  • Modulating miR-145 presents a potential therapeutic strategy for osteoarthritis.
Keywords:
FRS2OsteoarthritisPI3K/Akt/Mtorautophagychondrocytes.miR-145

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