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ナカシマ カズヒサ
Nakashima Kazuhisa
中島 和久 所属 鶴見大学 歯学部 歯学科 薬理学 職種 准教授 |
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| 論文種別 | 【査読あり】 研究論文（学術雑誌） |
| 言語種別 | 英語 |
| 査読の有無 | 査読あり |
| 表題 | Constitutively active parathyroid hormone receptor signaling in cells in osteoblastic lineage suppresses mechanical unloading-induced bone resorption |
| 掲載誌名 | 正式名：JOURNAL OF BIOLOGICAL CHEMISTRY ISSNコード：00219258 |
| 出版社 | AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC |
| 巻・号・頁 | 282(35),pp.25509-25516 |
| 著者・共著者 | Noriaki Ono,Kazuhisa Nakashima,Ernestina Schipani,Tadayoshi Hayata,Yoichi Ezura,Kunimichi Soma,Henry M. Kronenberg,Masaki Noda |
| 発行年月 | 2007/08 |
| 概要 | Multiple signaling pathways participate in the regulation of bone remodeling, and pathological negative balance in the regulation results in osteoporosis. However, interactions of signaling pathways that act comprehensively in concert to maintain bone mass are not fully understood. We investigated roles of parathyroid hormone receptor ( PTH/PTHrP receptor) signaling in osteoblasts in unloading-induced bone loss using transgenic mice. Hind limb unloading by tail suspension reduced bone mass in wild-type mice. In contrast, signaling by constitutively active PTH/PTHrP receptor ( caPPR), whose expression was regulated by the osteoblast-specific Col1a1 promoter ( Col1a1-caPPR), suppressed unloading-induced reduction in bone mass in these transgenic mice. In Col1a1-caPPR transgenic ( Tg) mice, hind limb unloading suppressed bone formation parameters in vivo and mineralized nodule formation in vitro similarly to those observed in wild-type mice. In addition, serum osteocalcin levels and mRNA expression levels of type I collagen, Runx2 and Osterix in bone were suppressed by unloading in both wild-type mice and Tg mice. However, in contrast to unloading-induced enhancement of bone resorptio |
| DOI | 10.1074/jbc.M610782200 |
| PMID | 17500070 |