Role of Interleukin-6 in Uncoupling of Bone In Vivo in a Human Squamous Carcinoma Coproducing Parathyroid Hormone-Related Peptide and Interleukin-6
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- Yumiko Nagai
- Biomedical Research Laboratories, Kureha Chemical Industry, Co., Ltd., Tokyo, Japan
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- Hideyuki Yamato
- Biomedical Research Laboratories, Kureha Chemical Industry, Co., Ltd., Tokyo, Japan
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- Keiko Akaogi
- Biomedical Research Laboratories, Kureha Chemical Industry, Co., Ltd., Tokyo, Japan
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- Kunitaka Hirose
- Biomedical Research Laboratories, Kureha Chemical Industry, Co., Ltd., Tokyo, Japan
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- Yoshito Ueyama
- Central Institute for Experimental Animals, Kanagawa, Japan
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- Kyoji Ikeda
- Department of Geriatric Research, National Institute for Longevity Sciences, Aichi, Japan
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- Toshio Matsumoto
- First Department of Internal Medicine, University of Tokushima School of Medicine, Tokushima, Japan
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- Toshiro Fujita
- Fourth Department of Internal Medicine, University of Tokyo School of Medicine, Tokyo, Japan
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- Etsuro Ogata
- Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan
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<jats:title>Abstract</jats:title> <jats:p>OCC tumor has been established from a human squamous carcinoma associated with humoral hypercalcemia of malignancy (HHM) and shown to overproduce parathyroid hormone-related peptide (PTHrP) and cause aggressive hypercalcemia when implanted into nude rats. In the present study, we have demonstrated by reverse transcription-polymerase chain reaction and Northern blot analysis that OCC tumor also overexpressed interleukin 6 (IL-6) mRNA and that tumor-bearing animals exhibited a marked increase in plasma IL-6 as well as PTHrP concentrations. When a monoclonal antibody against human IL-6 was injected to block the activities of tumor-derived IL-6, bone loss in tumor-bearing animals was significantly prevented. Quantitative bone histomorphometric analysis revealed that treatment with anti–IL-6 antibody caused a substantial decrease in both osteoclast number and eroded surface (as parameters of bone resorption) and also a significant increase in the mineral apposition rate, but little effect on the osteoblastic surface. These results provide in vivo evidence suggesting that in tumors coproducing IL-6 and PTHrP, IL-6 is involved not only in the acceleration of osteoclastic bone resorption but also, at least in part, in the suppression of osteoblastic functions in HHM syndrome.</jats:p>
収録刊行物
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- Journal of Bone and Mineral Research
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Journal of Bone and Mineral Research 13 (4), 664-672, 1998-04-01
Oxford University Press (OUP)
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詳細情報
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- CRID
- 1361699993981576192
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- NII論文ID
- 30021656396
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- NII書誌ID
- AA10688587
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- ISSN
- 15234681
- 08840431
- http://id.crossref.org/issn/08840431
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