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Arthritis
Volume 2012 (2012), Article ID 648537, 7 pages
http://dx.doi.org/10.1155/2012/648537
Research Article

Expression of Angiotensin II Receptor-1 in Human Articular Chondrocytes

1Department of Biochemistry, Institute of Medical Science, St. Marianna University School of Medicine, Kawasaki-shi, Kanagawa 2168511, Japan
2Department of Orthopaedic Surgery, School of Medicine, Yokohama City University, Yokohama-shi, Kanagawa 2360004, Japan
3Department of Frontier Medicine, Institute of Medical Science, St. Marianna University School of Medicine, Kawasaki-shi, Kanagawa 2168512, Japan
4Department of Joint Disease and Rheumatism, Nippon Medical School, Bunkyo-ku, Tokyo 1138603, Japan
5Department of Orthopaedic Surgery, St. Marianna University School of Medicine, Kawasaki-shi, Kanagawa 2168511, Japan
6Graduate School of Nutritional Science, Sagami Women's University, Sagamihara-shi, Kanagawa 2520383, Japan

Received 10 August 2012; Revised 21 November 2012; Accepted 5 December 2012

Academic Editor: George D. Kitas

Copyright © 2012 Yuki Kawakami et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background. Besides its involvement in the cardiovascular system, the renin-angiotensin-aldosterone (RAS) system has also been suggested to play an important role in inflammation. To explore the role of this system in cartilage damage in arthritis, we investigated the expression of angiotensin II receptors in chondrocytes. Methods. Articular cartilage was obtained from patients with osteoarthritis, rheumatoid arthritis, and traumatic fractures who were undergoing arthroplasty. Chondrocytes were isolated and cultured in vitro with or without interleukin (IL-1). The expression of angiotensin II receptor types 1 (AT1R) and 2 (AT2R) mRNA by the chondrocytes was analyzed using reverse transcription-polymerase chain reaction (RT-PCR). AT1R expression in cartilage tissue was analyzed using immunohistochemistry. The effect of IL-1 on AT1R/AT2R expression in the chondrocytes was analyzed by quantitative PCR and flow cytometry. Results. Chondrocytes from all patient types expressed AT1R/AT2R mRNA, though considerable variation was found between samples. Immunohistochemical analysis confirmed AT1R expression at the protein level. Stimulation with IL-1 enhanced the expression of AT1R/AT2R mRNA in OA and RA chondrocytes. Conclusions. Human articular chondrocytes, at least partially, express angiotensin II receptors, and IL-1 stimulation induced AT1R/AT2R mRNA expression significantly.