Silencing of endocan down-regulates the expression of angiogenesis-associated genes in IL-1ß activated chondrocytes

PURPOSE: to investigate endocan expression and the underlying molecular mechanisms in human chondrocytes stimulated with IL-1β. METHODS: chondrocytes were cultured and stimulated with IL-1β. A separate set of chondrocytes were incubated with a specific NF-kB inhibitor or a small interfering RNA against endocan mRNA before IL-1β. addition. Endocan, VEGFR-2 and ERK expression were evaluated. RESULTS: IL-1β.was able to increase significantly endocan expression as well as NF-kB activity. On the contrary, in chondrocytes treated with NF-kB inhibitor , the effects of IL-1β on endocan expression was significantly reduced. In endocan knockdown cells we found a decrease in VEGF signaling pathways. DISCUSSION: endocan was found highly expressed in arthritic synovial tissues from patients with rheumatoid arthritis or osteoarthritis. In these settings, endocan could be involved in the mechanisms that stimulate cell invasion, cell migration, and angiogenesis in the pannus of arthritic joints. Our data, clearly demonstrate that endocan is part of inflammatory response in chondrocytes and in turn is involved in the modulation of proangiogenic factors. Conclusion: Endocan released by activated chondrocytes may be involved in the mechanisms that stimulate cell migration and invasion as well as angiogenesis in the pannus of arthritic joints.