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Neuron/Glial Antigen 2-Type VI Collagen Interactions During Murine Temporomandibular Joint Osteoarthritis

Mamoru Yotsuya1,2, Andrew E Bertagna1, Nageeb Hasan1

  • 1University of Illinois at Chicago, Department of Oral Biology, Chicago, IL, USA.

Scientific Reports
|January 13, 2019
PubMed

Insights

Neuron/glia antigen 2 (NG2) interactions with type VI collagen are altered in temporomandibular joint osteoarthritis (TMJ-OA). Increased cytosolic NG2 in TMJ-OA suggests a novel molecular mechanism in chondrocyte dysfunction.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Orthopedics

Background:

  • Temporomandibular joint osteoarthritis (TMJ-OA) involves articular cartilage degeneration driven by signaling pathway disruptions.
  • Cell-matrix interactions, particularly involving type VI collagen and Neuron/glia antigen 2 (NG2), play a role in chondrocyte function.
  • Understanding these interactions is crucial for elucidating TMJ-OA pathogenesis.

Purpose of the Study:

  • To define the temporospatial dynamics of NG2-type VI collagen interactions during TMJ-OA progression.
  • To investigate the cellular localization and transport mechanisms of NG2 in the context of TMJ-OA.
  • To explore the potential of NG2 as a novel molecular marker or therapeutic target in TMJ-OA.

Main Methods:

  • Utilized a surgical instability model to induce TMJ-OA in the mandibular condylar cartilage (MCC).
  • Examined the colocalization of NG2 and type VI collagen in superficial, chondroblastic, and hypertrophic chondrocytes.
  • Investigated NG2 transport via clathrin and dynamin-mediated endocytic pathways.

Main Results:

  • Membrane-bound NG2 colocalizes with pericellular type VI collagen in superficial MCC cells.
  • High levels of cytosolic NG2 were observed in chondroblastic and hypertrophic cells.
  • TMJ-OA induction led to disrupted pericellular type VI collagen and increased cytosolic NG2 in central/medial MCC.
  • Cytosolic NG2 transport occurs through clathrin and dynamin-mediated endocytosis.

Conclusions:

  • NG2 exhibits distinct cellular localization patterns in MCC, shifting to the cytosol during TMJ-OA progression.
  • Disruptions in pericellular type VI collagen are associated with increased cytosolic NG2 in TMJ-OA.
  • NG2's endocytic transport mechanism in TMJ-OA chondrocytes highlights its potential role in disease pathogenesis.
  • NG2 represents a novel molecular mechanism linked to chondrocyte dysfunction in TMJ-OA.

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