Loss of adseverin, an actin binding protein, in an animal model of osteoarthritis

Abstract

Purpose: Articular cartilage health and function is largely dependent on the stability of the chondrocyte phenotype. In healthy articular cartilage, chondrocytes are fine-tuned to balance between anabolic and catabolic functions to maintain the extracellular matrix. In osteoarthritis (OA) however, a disease characterized by the progressive degradation of the cartilage matrix, the articular chondrocyte phenotype is lost. As a result, these cells decrease the expression of chondrogenic matrix molecules such as aggrecan and collagen type II while increasing the expression of matrix degrading enzymes like matrix metalloproteinase 13 (MMP13).The pro-inflammatory cytokines interleukin 1 beta (IL-1β) and tumor necrosis factor alpha (TNFα) have been implicated as key mediators in the pathogenesis of osteoarthritis (OA) and have been shown to be increased in the cartilage tissues of the murine destabilization of the medial meniscus (DMM) model of OA.