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Endocrinology Vol. 138, No. 11 4959-4965
Copyright © 1997 by The Endocrine Society

ARTICLES

Osteoclasts Are Present in gp130-Deficient Mice1

Kojiro Kawasaki2, Yu-Hao Gao, Satoshi Yokose3, Yoshio Kaji, Toshitaka Nakamura, Tatsuo Suda, Kanji Yoshida, Tetsuya Taga4, Tadamitsu Kishimoto, Hiroko Kataoka, Takahito Yuasa, Hiromichi Norimatsu and Akira Yamaguchi

Departments of Oral Pathology (K.K., Y.G., S.Y., H.K., T.Y., A.Y.) and Biochemistry (T.S.), School of Dentistry, Showa University, Tokyo 142, Japan; Department of Orthopedic Surgery (K.K., H.N.), Kagawa Medical School, Kagawa 761–07, Japan; Department of Orthopedic Surgery (T.N.), School of Medicine, University of Occupational and Environmental Health, Fukuoka 807, Japan; Institute for Molecular and Cellular Biology (K.Y., T.T.), Osaka University, Osaka 565, Japan; Department of Medicine III (T.K.), Osaka University Medical School, Osaka 565, Japan; and Department of Orthopedic Surgery (T.Y.), Juntendo University School of Medicine, Tokyo, Japan

Address all correspondence and requests for reprints to: Akira Yamaguchi, Department of Oral Pathology, School of Dentistry, Showa University, 1–5-8 Hatanodai, Shinagawa-ku, Tokyo 142, Japan. E-mail: akirayam{at}dent.showa-u.ac.jp

Interleukin (IL)-6, IL-11, leukemia inhibitory factor, and oncostatin M similarly induce osteoclast formation in cocultures of osteoblastic cells and bone marrow cells. These cytokines share a common signal transducer, gp130, which forms a receptor complex with the specific receptor for each cytokine. To investigate the role of gp130 in osteoclast development, we examined bone tissues in gp130-deficient and wild-type newborn mice of the ICR background. Soft x-ray radiographs and microfocus x-ray computed tomographs revealed that bone marrow cavities were present in tibiae and radii of both wild-type and gp130-deficient mice. Microfocus x-ray computed tomography and histological examination demonstrated a decrease in the amount of trabeculae at the metaphysial region in tibiae and radii of the gp130-deficient mice compared with the wild-type mice. The number of osteoclasts in gp130-deficient mice was about double that in the wild-type mice. There were no apparent differences in the distributions of alkaline phosphatase-positive osteoblasts and the osteoid surface on the trabecular bone at the metaphysial region between the wild-type and gp130-deficient mice. The volume of mineralized trabecular bones was also decreased at mandibulae, accompanied by the increased number of osteoclasts in gp130-deficient mice compared with the wild-type and heterozygous mice. These results suggest that the formation of osteoclasts is not solely dependent on gp130 signaling, at least during fetal development. The osteoclastic bone resorption in gp130-deficient mice may be caused by the functional redundancy of bone-resorbing hormones and cytokines other than those of the IL-6 family.




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