Interleukin (IL)-6 induction of osteoclast differentiation depends on IL-6 receptors expressed on osteoblastic cells but not on osteoclast progenitors.
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- N Udagawa
- Department of Biochemistry, School of Dentistry, Showa University, Tokyo, Japan.
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- N Takahashi
- Department of Biochemistry, School of Dentistry, Showa University, Tokyo, Japan.
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- T Katagiri
- Department of Biochemistry, School of Dentistry, Showa University, Tokyo, Japan.
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- T Tamura
- Department of Biochemistry, School of Dentistry, Showa University, Tokyo, Japan.
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- S Wada
- Department of Biochemistry, School of Dentistry, Showa University, Tokyo, Japan.
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- D M Findlay
- Department of Biochemistry, School of Dentistry, Showa University, Tokyo, Japan.
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- T J Martin
- Department of Biochemistry, School of Dentistry, Showa University, Tokyo, Japan.
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- H Hirota
- Department of Biochemistry, School of Dentistry, Showa University, Tokyo, Japan.
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- T Taga
- Department of Biochemistry, School of Dentistry, Showa University, Tokyo, Japan.
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- T Kishimoto
- Department of Biochemistry, School of Dentistry, Showa University, Tokyo, Japan.
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- T Suda
- Department of Biochemistry, School of Dentistry, Showa University, Tokyo, Japan.
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Abstract
<jats:p>We reported that interleukin (IL) 6 alone cannot induce osteoclast formation in cocultures of mouse bone marrow and osteoblastic cells, but soluble IL-6 receptor (IL-6R) strikingly triggered osteoclast formation induced by IL-6. In this study, we examined the mechanism of osteoclast formation by IL-6 and related cytokines through the interaction between osteoblastic cells and osteoclast progenitors. When dexamethasone was added to the cocultures, IL-6 could stimulate osteoclast formation without the help of soluble IL-6R. Osteoblastic cells expressed a very low level of IL-6R mRNA, whereas fresh mouse spleen and bone marrow cells, both of which are considered to be osteoclast progenitors, constitutively expressed relatively high levels of IL-6R mRNA. Treatment of osteoblastic cells with dexamethasone induced a marked increase in the expression of IL-6R mRNA. By immunoblotting with antiphosphotyrosine antibody, IL-6 did not tyrosine-phosphorylate a protein with a molecular mass of 130 kD in osteoblastic cells but did so in dexamethasone-pretreated osteoblastic cells. Osteoblastic cells from transgenic mice constitutively expressing human IL-6R could support osteoclast development in the presence of human IL-6 alone in cocultures with normal spleen cells. In contrast, osteoclast progenitors in spleen cells from transgenic mice overexpressing human IL-6R were not able to differentiate into osteoclasts in response to IL-6 in cocultures with normal osteoblastic cells. These results clearly indicate that the ability of IL-6 to induce osteoclast differentiation depends on signal transduction mediated by IL-6R expressed on osteoblastic cells but not on osteoclast progenitors.</jats:p>
Journal
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- The Journal of experimental medicine
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The Journal of experimental medicine 182 (5), 1461-1468, 1995-11-01
Rockefeller University Press
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Details 詳細情報について
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- CRID
- 1361137045680956672
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- NII Article ID
- 30017433088
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- NII Book ID
- AA00697559
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- ISSN
- 15409538
- 00221007
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- Data Source
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- Crossref
- CiNii Articles