Provo, UT 84602
Physiology & Developmental Biology
The long-term goal of our lab is to identify and characterize molecular activities that are common to many or possibly all pathways of osteoarthritis (OA) cartilage degeneration, in order to identify potential targets for drug development. Our objectives include to determine the extent to which three molecular pathways that have been identified as possible contributors to OA, the discoidin domain receptor 2 (Ddr2) mediated activation of matrix metalloproteinase-13 (Mmp13), receptor for advanced glycation end-products (RAGE) associated inflammation, and the unfolded protein stress response (UPR), participate in the progression of OA in genetic and induced injury mouse models of OA.
The central hypothesis of our work is that the HtrA1/Ddr2/Mmp13 pathway, initiated by inflammation, drives the degradation of articular cartilage in both genetic and injury mouse OA models, while the UPR is a separable effect that is not essential for cartilage degeneration.