Conclusion
Intact TGFBR2 signalling drives early and worse knee OA in itga1-null mice. This result supports the hypothesis that the increased expression of integrin α1β1 by superficial zone chondrocytes early in OA development dampens TGFBR2 signalling and thus protects against degeneration.
Methods
Behavioural and histological manifestations of spontaneous knee OA were measured at 4, 8, 12 and 16 months in mice with and without a ubiquitous itga1 deletion and with and without a tamoxifen-induced cartilage specific TGFBR2 depletion.
Results
Knee cartilage degeneration, collateral ligament ossification and pain responses increased with age. Itga1-null mice with intact TGFBR2 signalling developed earlier and more severe OA compared to controls. In agreement with our hypothesis, depleting TGFBR2 signalling in the cartilage of itga1-null mice attenuated OA progression.