2009 Fiscal Year Final Research Report

Study of osteoclast activating factor when mechanical stress changes through osteoblast controlled by osteocyte

Research Project

Project/Area Number	20791047
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Single-year Grants
Research Field	Orthopaedic surgery
Research Institution	Nagasaki University
Principal Investigator	(MORIISHI Takeshi Nagasaki University, 大学院・医歯薬学総合研究科, 技術職員 (20380983)
Project Period (FY)	2008 – 2009
Keywords	力学的負荷 / 骨細胞 / 骨芽細胞 / 破骨細胞活性化因子
Research Abstract	We established human Bcl-2 transgenic mice under the control of mouse 2.3 kb Col1a1 promoter. Osteocyte processes were reduced depending on the expression levels of the transgene and they were sparsely connected with each other in Bcl-2 transgenic mice. At the unloaded condition, bone mass decreased in wild-type mice due to impaired osteoblast function and enhanced osteoclastogenesis through RANKL induction but not in Bcl-2 transgenic mice. These findings show that osteocytes negatively regulate bone mass by inhibiting osteoblast function and activating osteoclastogenesis and these functions are augmented at the unloaded condition. Moreover, osteocyte expression gene analysis using microarray showed that 5322 genes are chang in Runx2 transgenic mice (Dev Biol. 2006 Aug 1 ; 296 (1) : 48-61), at unloaded condition. Our findings will provide the basis for the understanding of the osteocyte network, which plays an important role in the regulation of bone mass.