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 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