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Cyclic Compression Loaded on Cartilage Explants Enhances the Production of Reactive Oxygen Species
TAKASHI TOMIYAMA, KANJI FUKUDA, KENJI YAMAZAKI, KAZUKI HASHIMOTO, HIRONOBU UEDA, SHIGESHI MORI, and CHIAKI HAMANISHI ABSTRACT. Objective. Although mechanical forces are an essential factor in the regulation of cartilage metabolism, the precise mechanisms involved have not yet been determined. We previously demonstrated that mechanical forces on chondrocytes inhibited proteoglycan (PG) synthesis. We also demonstrated the induction of reactive oxygen species (ROS) is loaded on the chondrocytes. Our purpose was to determine the ROS induction with mechanical compression and its involvement in PG synthesis of cartilage slices. Methods. Bovine articular cartilage slices were subjected to cyclic compression loading. Synthesis of PG and ROS was measured using Na2[35S]-SO4 and a chemiluminescent probe, respectively. The induction of nitrotyrosine was determined using immunohistochemistry. Results. The synthesis of PG was significantly inhibited with 2.0 MPa of compression stress; 1 h of compression was sufficient to inhibit PG synthesis. The ROS inhibitor ebselen reversed the compression-inhibited synthesis of PG. Compression on the cartilage induced synthesis of ROS and the expression of nitrotyrosine. Conclusion. Mechanical compression at 2.0 MPa inhibited PG synthesis by cartilage explants. ROS were involved in this action. (First Release Feb 15 2007; J Rheumatol 2007;34:556–62) Key Indexing Terms:
COMPRESSION From the Department of Orthopaedic Surgery, Kinki University School of Medicine, Osaka, Japan. Supported by a research grant from the Scientific Research Fund of the Ministry of Education, Science and Culture of Japan. T. Tomiyama, MD, PhD; K. Fukuda, MD, PhD; K. Yamazaki, MD, PhD; K. Hashimoto, MD, PhD; H. Ueda, MD, PhD; S. Mori, MD, PhD; C. Hamanishi, MD, PhD, Department of Orthopaedic Surgery, Kinki University School of Medicine. Address reprint requests to Dr. K. Fukuda, Department of Orthopaedic Surgery, Kinki University School of Medicine, 377-2 Ohno-higashi, Osaka-sayama, Osaka 589-8511, Japan. E-mail: k-fukuda@med.kindai.ac.jp Accepted for publication November 6, 2006.
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