|
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 |
|
| 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 | Transient receptor potential vanilloid 4 deficiency suppresses unloading-induced bone loss |
| 掲載誌名 | 正式名：Journal of Cellular Physiology ISSNコード：00219541 |
| 巻・号・頁 | 216(1),pp.47-53 |
| 著者・共著者 | Fumitaka Mizoguchi,Atsuko Mizuno,Tadayoshi Hayata,Kazuhisa Nakashima,Stefan Heller,Takashi Ushida,Masahiro Sokabe,Nobuyuki Miyasaka,Makoto Suzuki,Yoichi Ezura,Masaki Noda |
| 発行年月 | 2008/07 |
| 概要 | Mechanosensing is one of the crucial components of the biological events. In bone, as observed in unloading-induced osteoporosis in bed ridden patients, mechanical stress determines the levels of bone mass. Many molecules have been suggested to be involved in sensing mechanical stress in bone, while the full pathways for this event has not yet been identified. We examined the role of TRPV4 in unloading-induced bone loss. Hind limb unloading induced osteopenia in wild-type mice. In contrast, TRPV4 deficiency suppressed such unloading-induced bone loss. As underlying mechanism for such effects, TRPV4 deficiency suppressed unloading-induced reduction in the levels of mineral apposition rate and bone formation rate. In these mice, unloading-induced increase in the number of osteoclasts in the primary trabecular bone was suppressed by TRPV4 deficiency. Unloading-induced reduction in the longitudinal length of primary trabecular bone was also suppressed by TRPV4 deficiency. TRPV4protein is expressed in both osteoblasts and osteoclasts. These results indicated that TRPV4 plays a critical role in unloading-induced bone loss. © 2008 Wiley-Liss, Inc. |
| DOI | 10.1002/jcp.21374 |
| PMID | 18264976 |