Why this study matters

Understanding the pathologic process underlying OA will facilitate the development of molecular-based therapies.

Study design

Proteins were extracted from homogenized cartilage samples obtained from patients (n=11) and rabbits with OA (n=12).

Glycopatterns and the expression of fucosyltransferases were determined, and tumor necrosis factor receptor superfamily member 1A (TNFR1) binding to TNF-α was assessed relative to α-1,3 fucosylation.

Results and conclusion

TNF-α induced α-1,3 fucosylation in cartilage and chondrocytes obtained from patients and rabbits with OA. This effect was mediated by overexpression of FUT10.

Blocking FUT10 expression inhibited binding of TNF-α to TNFR1, which decreased ECM degradation.