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Targeted mutation of NOV/CCN3 in mice disrupts joint homeostasis and causes osteoarthritis-like disease

K A Roddy1, C A Boulter1

  • 1School of Biosciences, Cardiff University, Museum Avenue, Cardiff CF10 3AX, UK.

Osteoarthritis and Cartilage
|December 27, 2014
PubMed
Abstract

Insights

The matricellular protein NOV is essential for maintaining joint health. Its absence in aging mice leads to severe osteoarthritis-like joint degeneration, highlighting NOV

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Orthopedics

Background:

  • The matricellular protein NOV/CCN3 is implicated in osteoarthritis (OA).
  • Targeted mutation of NOV in mice (Nov(del3)) results in joint abnormalities.

Purpose of the Study:

  • To investigate if NOV is required for maintaining joint homeostasis.
  • To determine if NOV disruption causes joint degeneration.

Main Methods:

  • Characterization of NOV expression in adult mouse joints via immunohistochemistry.
  • Comparative analysis of Nov(del3)-/- and wild-type mice joints (2, 6, 12 months) using X-ray, histology, and immunohistochemistry.

Main Results:

  • NOV protein is present in articular cartilage, meniscus, synovium, and ligament attachment sites.
  • Nov(del3)-/- males developed severe OA-like pathology by 12 months, including cartilage erosion and osteophytes.
  • Articular cartilage cell density was altered in Nov(del3)-/- mice, decreasing significantly by 6 and 12 months in both sexes.

Conclusions:

  • NOV is crucial for maintaining articular cartilage integrity and overall joint homeostasis.
  • Disruption of NOV in aging Nov(del3)-/- male mice leads to osteoarthritis-like disease.
Keywords:
Joint homeostasisNOV/CCN3OsteoarthritisTargeted mouse mutant

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