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 | Runx2 is a target of mechanical unloading to alter osteoblastic activity and bone formation in vivo |
掲載誌名 | 正式名:ENDOCRINOLOGY ISSNコード:00137227 |
出版社 | ENDOCRINE SOC |
巻・号・頁 | 147(5),pp.2296-2305 |
著者・共著者 | R Salingcarnboriboon,K Tsuji,T Komori,K Nakashima,Y Ezura,M Noda |
発行年月 | 2006/05 |
概要 | Molecular mechanisms underlying unloading-induced reduction of bone formation have not yet been fully understood. In vitro, Runx2 has been suggested to be involved in mechanical signaling in osteoblasts. However, the roles of Runx2 in vivo during the bone response to mechanical stimuli have not yet been known. The purpose of this paper was to examine the roles of Runx2 in unloading-induced bone loss in vivo. Tail suspension was conducted for 2 wk using 9- to 11-wk-old Runx2 heterozygous knockout mice (Runx2(+/-)) and wild-type (Wt) littermates. Bones were subjected to two-dimensional micro-x-ray computed tomography, bone histomorphometry and RT-PCR analyses. Loss of half Runx2 gene dosage-exacerbated unloading-induced bone loss in trabecular and cortical envelopes. Unloading-induced reduction in mineral apposition rate and bone formation rate in cortical bone as well as trabecular bone was exacerbated in Runx2(+/-) mice, compared with Wt mice. Bone resorption parameters were not significantly affected by unloading or Runx2(+/-) genotype. Basal Runx2 and osterix mRNA levels in bone were reduced by 50% in Wt, whereas unloading in Runx2(+/-) mice did not further alter Runx2 and osteri |
DOI | 10.1210/en.2005-1020 |
PMID | 16455780 |