Upregulation of arginase-II in osteoarthritic chondrocytes:

Abstract

Osteoarthritis (OA) is characterized by cartilage destruction and occurs to be related to various metabolic disorders. However, in OA pathogenesis, mechanism of pathological effect of amino acids has not been clearly identified to date. We herein demonstrate that alterations of amino acid metabolism are important to OA pathogenesis in mice. Our microarray analysis showed that arginase-II (Arg-II) expression was significantly increased in mouse chondrocytes under various osteoarthritic conditions. Arg-II was also upregulated in mouse OA chondrocytes induced by various catabolic regulators and in OA cartilage of human and various mouse models. Moreover, Arg-II overexpressed by using Adenoviral systems in mouse chondrocytes and knee joint tissues lead to OA pathogenesis. Our findings demonstrate that Arg-II is a novel catabolic regulator of OA pathogenesis and could be a potential therapeutic target for the treatment of OA.