Possible function of haptoglobin in osteoarthritis pathogenesis

Abstract

Osteoarthritis (OA) is a complicated disease which is caused by various risk factors such as aging, obestiy, and traumatic injury. Despite its high socioeconomic burden, there is no available disease-modifying OA theraphy to date. Therefore, discovery of OA biomarker is important for the early diagnosis of OA pathogenesis. One of candidates for biomarker is haptoglobin (HP) that is highly expressed in OA patients. However, the role of HP in OA pathogenesis has not been investigated yet. Therefore, this study is performed to characterize the function of HP in OA pathogenesis. Cell-based studies reveal that overexpression of HP alone did not alter the expression levels of matrix-degrading-enzymes and cartilage extracellular matrix molecules. However, overexpression of HP slightly inhibited expression of MMPs induced by HIF-2α in mouse chondrocytes. Futhermore, in vivo studies demonstrate that adenovirus-mediated overexpression of HP in mouse knee joint tissues did not induce OA pathogenesis and modulate ctilage destruction induced by HIF-2α overexpression. On the other hand, osteophyte formation and maturity tend to be slightly alleviated in HP knockout mice compared to wild-type mice. This studies indicate that HP may play a potential role in OA pathogenesis.