Glycophenotyping of osteoarthritic fibroblast-like synoviocytes

Abstract

Purpose: Our previous research brought evidence that the pathogenesis of osteoarthritis (OA) is linked to alterations in the glycobiology of articular cartilage. As such, distinct glycan structures are altered in OA cartilage with progressing degeneration, accompanied by the over-representation of specific galectins in affected chondrocytes. As a result of the modified glycan-galectin interaction under OA conditions, clinically relevant inflammatory-response genes and matrix metalloproteinases are upregulated in OA chondrocytes via NF-κB signaling.