Page 28 - N. Metabolism and metabolic diseases
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[N. Metabolism and metabolic diseases-15]



              Carbonic anhydrase regulates anabolic and catabolic factors


                                         in articular chondrocytes




        Yunhui Min¹, Dahye Kim², Dinesh Suminda Godagama Gamaarachchige¹, Xiangyu Zhao¹, Mangeun Kim²,
                                                    Young-Ok Son¹˙²˙*


         ¹Interdisciplinary Graduate Program in Advanced Convergence Technology and Science, Jeju National University,

         Jeju 63243, Republic of Korea, ²Animal Biotechnology, Faculty of Biotechnology, College of Applied Life Sciences,
                                    Jeju National University, Jeju 63243, Republic of Korea




        Osteoarthritis (OA) is caused by imbalance of anabolic and catabolic factors. An articular cartilage is one of the

        most avascular tissue and it is relatived with the hypoxic and acidic milieu. Carbonic anhydrases (CA) enzymes are
        zinc-containing metalloenzymes that catalyze reversible hydration-dehydration of carbon dioxide and bicarbonate.

        Therefore, CA is important for the regulation of acid-base status in the cells. However, a little information is available
        about the effects of pH imbalance in cartilage degeneration. Here, we investigated the roles of pH imbalance in

        cartilage degeneration in chondrocytes by focusing on the CA enzymes. Microarray analysis revealed that among
        16  CA  family  members,  Car9,  Car12,  and  Car13  are  specifically  upregulated  in  OA  chondrocytes.  We  further

        confirmed the microarray data by the RT-PCR. Moreover, adenovirus-mediated overexpression of Car9, Car12 and
        Car13 modulates anabolic or catabolic factors in articular chondrocytes. Adenovirus-mediated overexpression of

        Car9, Car12, and Car13 in mouse knee-joint tissue also modulates OA pathogenesis. Taken together, these results
        suggested that CA might be new key factors in cartilage degeneration where pH imbalance is an important mediator

        in OA pathogenesis.
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