Rachel W Li
Australian National University Medical School, Australia
Title: Heparanase and inflammatory mediators in Rheumatoid arthritis (RA)
Biography
Biography: Rachel W Li
Abstract
Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by synovial inflammation in multiple joints with hyperplasia of the synovial intimal lining layer, influx of inflammatory cells and angiogenesis, eventually resulting in the destruction of cartilage and bone. The early process of angiogenesis is recognized as a fundamental process in pannus formation. Given that angiogenesis is one of the earliest manifestations in RA, the ability to determine a marker for angiogenesis and demonstrate its specificity in RA would aid in disease diagnosis. Despite the diagnostic contribution of currently used RA markers and rheumatoid factors, about one-third of RA patients remain seronegative. Heparanase (HPSE) activity is implicated in promotion of angiogenesis in the synovium and RA progression. The action of heparanase is involved in multiple regulatory events related, among other effects, to augmented bioavailability of growth factors and cytokines at sites of inflammation, allowing extravasation of immune cells into nonvascular spaces and releasing inflammatory mediators that regulate angiogenesis. We reported a highly significant increase of HPSE activity and expression in synovial fluid and synovial tissue of RA patients, and the increase of the heparanase activity positively correlates with angiogenic gene expression. We have further obtained preliminary evidence from which we postulate that the involvement of HPSE in gene regulation in the development of pannus in RA may be reflected in the patients’ blood, which makes heparanase a potential predictor of RA progression and a novel therapeutic target in RA.