Journal
BIOMOLECULES
Volume 13, Issue 5, Pages -Publisher
MDPI
DOI: 10.3390/biom13050851
Keywords
endocan; proteoglycans; chondrocytes; inflammation; angiogenic factors
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Increased endocan expression was found in arthritic patients and chondrocytes stimulated with IL-1ss. The knockdown of endocan significantly reduced the expression of pro-angiogenic molecules and NF-kB activation in IL-1ss-induced inflammation, suggesting a role for endocan in the mechanisms of cell migration, invasion, and angiogenesis in arthritic joints.
Endocan is a small soluble proteoglycan (PG) known to be involved in inflammation and angiogenesis. Increased endocan expression was found in the synovia of arthritic patients and chondrocytes stimulated with IL-1ss. Considering these findings, we aimed to investigate the effects of endocan knockdown on the modulation of pro-angiogenic molecules expression in a model of IL-1ss-induced inflammation in human articular chondrocytes. Endocan, VEGF-A, MMP-9, MMP-13, and VEGFR-2 expression was measured in both normal and endocan knockdown chondrocytes stimulated with IL-1ss. VEGFR-2 and NF-kB activation were also measured. Results have shown that endocan, VEGF-A, VEGFR-2, MMP-9, and MMP-13 were significantly up-regulated during IL-1ss-induced inflammation; interestingly, the expression of such pro-angiogenic molecules and NF-kB activation were significantly reduced by endocan knockdown. These data support the hypothesis that 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.
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