DUSP4 alleviates LPS-induced chondrocyte injury in knee osteoarthritis via the MAPK signaling pathway

Zhengnan Li1, Bojie Chen2

  • 1Department of Sports Medicine, Ganzhou People's Hospital, Zhanggong, Jiangxi 341000, P.R. China.

Insights

Dual specificity protein phosphatase 4 (DUSP4) is decreased in knee osteoarthritis (KOA). Overexpressing DUSP4 protects chondrocytes from injury by inhibiting the MAPK pathway, reducing inflammation and apoptosis.

Area of Science:

  • Biomedical research
  • Cell biology
  • Molecular mechanisms of disease

Background:

  • Knee osteoarthritis (KOA) involves complex cartilage damage pathogenesis.
  • Dual specificity protein phosphatase 4 (DUSP4) expression is reduced in osteoarthritis (OA).
  • The precise function and mechanism of DUSP4 in OA remain unclear.

Purpose of the Study:

  • To investigate the role and mechanism of DUSP4 in knee osteoarthritis.
  • To determine if DUSP4 affects chondrocyte viability, oxidative stress, inflammation, and apoptosis.
  • To elucidate the involvement of the MAPK signaling pathway in DUSP4's function in OA.

Main Methods:

  • Established an OA cell injury model using ATDC5 cells treated with lipopolysaccharide (LPS).
  • Quantified DUSP4 expression using reverse transcription-quantitative PCR and western blot.
  • Assessed cell viability, oxidative stress, inflammation, and apoptosis via Cell Counting Kit-8, ELISA, TUNEL, and western blotting assays.
  • Investigated the MAPK pathway's role using a specific agonist (PMA).

Main Results:

  • DUSP4 expression was significantly decreased in OA chondrocytes.
  • Overexpression of DUSP4 inhibited LPS-induced chondrocyte injury.
  • DUSP4 overexpression suppressed the MAPK signaling pathway, reducing oxidative stress, inflammation, and apoptosis.
  • MAPK pathway activation reversed the protective effects of DUSP4.

Conclusions:

  • DUSP4 plays a protective role in knee osteoarthritis.
  • DUSP4 alleviates LPS-induced chondrocyte injury in KOA.
  • The protective mechanism involves the inhibition of the MAPK signaling pathway.