Mary B. Goldring1
1Weill
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.