CD44 and cartilage matrix stabilization

One prominent feature of osteoarthritic cartilage is an inherent failure to retain a proteoglycan-rich extracellular matrix. This lack of retention occurs even as the chondrocytes respond with episodes of pronounced matrix biosynthesis. Thus, osteoarthritis is likely manifested in part by the inability of chondrocytes to retain matrix at the cell surface. Another aspect of degenerative changes in osteoarthritis is enhanced catabolism, often termed chondrocytic chondrolysis. Although many facets of chondrocyte catabolism and attempted repair have been extensively investigated, the signals that initiate such metabolic changes remain unclear. Matrix receptors direct the assembly and retention of the pericellular matrix and provide a linkage to the cytoskeleton. CD44 is the principal receptor for hyaluronan (HA) expressed by chondrocytes [1, 2, 3]. The interactions between matrix components and receptors establish a cell-associated pool of extracellular matrix molecules. These associations have the potential to signal changes in cell behavior, such as proliferation, apoptosis and matrix biosynthesis or turnover. In addition to chondrocyte integrins [4],CD44 represents another class of receptors that can participate in these matrix-cell-cytoskeleton interactions [3,5].