Mary B. Goldring1
Human cartilage is complex tissue of matrix proteins varying from superficial to deep layers and from loaded to unloaded zones. During OA development normally quiescent chondrocytes with low matrix turnover undergo phenotypic modulation causing matrix destruction and abnormal repair. We have been investigating mechanisms by which GADD45β, a stress response signaling molecule involved in cartilage development, and ESE-1, an inflammation-induced transcription factor, regulate collagen remodeling during osteoarthritis. Studies using human surgical specimens and mouse models of OA will elucidate how these factors disrupt cartilage homeostasis, leading to the development of targeted therapies that block cartilage damage, promoting effective repair.