High-Temperature Requirement A1 Protease as a Rate-Limiting Factor in the Development of Osteoarthritis.

Preserving the mature articular cartilage of joints is a critical focus in the prevention and treatment of osteoarthritis. We determined whether the genetic inactivation of high-temperature requirement A1 (HtrA1) can significantly attenuate the degradation of articular or condylar cartilage. Two types of mouse models of osteoarthritis were used, a spontaneous mutant mouse model [type XI collagen-haploinsufficient (Col11a1) mice] and two post-traumatic mouse models [destabilization of the medial meniscus (DMM) on the knee and a partial discectomy (PDE) on the temporomandibular joint].

Attenuation of the progression of articular cartilage degeneration by inhibition of TGF-β1 signaling in a mouse model of osteoarthritis.

Transforming growth factor beta 1 (TGF-β1) is implicated in osteoarthritis. We therefore studied the role of TGF-β1 signaling in the development of osteoarthritis in a developmental stage-dependent manner. Three different mouse models were investigated.

Pressure perturbation calorimetry of helical peptides.

Pressure perturbation calorimetry quantifies the temperature dependence of a solute's thermal expansion coefficient, providing information about solute-solvent interactions. We tested the idea that pressure perturbation calorimetry can provide information about solvent-accessible surface area by studying peptides with different secondary structures. The peptides comprised two host-guest series: one predominately an alpha-helix, the other predominately a polyproline II helix.