Chondroitin sulfate proteoglycans from salmon nasal cartilage inhibit angiogenesis

- The role of CSPGs in blood vessel formation in cartilage is largely unknown.
- Treatment of salmon PG inhibited in vitro and in vivo angiogenesis.
- The CS portion of salmon PG was responsible for the anti-angiogenic activity.
- Salmon PG also reduced MMP expression and inhibited cell adhesion.
- Our results support an anti-angiogenic role for CSPG in cartilage.

Because cartilage lacks nerves, blood vessels, and lymphatic vessels, it is thought to contain factors that inhibit the growth and development of those tissues. Chondroitin sulfate proteoglycans (CSPGs) are a major extracellular component in cartilage. CSPGs contribute to joint flexibility and regulate extracellular signaling via their attached glycosaminoglycan, chondroitin sulfate (CS). CS and CSPG inhibit axonal regeneration; however, their role in blood vessel formation is largely unknown. To clarify the function of CSPG in blood vessel formation, we tested salmon nasal cartilage proteoglycan (PG), a member of the aggrecan family of CSPG, for endothelial capillary-like tube formation. Treatment with salmon PG inhibited endothelial cell adhesion and in vitro tube formation. The anti-angiogenic activity was derived from CS in the salmon PG but not the core protein. Salmon PG also reduced matrix metalloproteinase expression and inhibited angiogenesis in the chick chorioallantoic membrane. All of these data support an anti-angiogenic role for CSPG in cartilage.