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

我们在小鼠2.3 kb Col1a1启动子的控制下建立了人Bcl-2转基因小鼠。在Bcl-2转基因小鼠中，骨细胞过程的减少取决于转基因的表达水平，并且它们之间相互稀疏连接。在空载条件下，野生型小鼠的骨量减少是由于成骨细胞功能受损和通过RANKL诱导的破骨细胞生成增强，而Bcl-2转基因小鼠则没有。这些研究结果表明，骨细胞通过抑制成骨细胞功能和激活破骨细胞生成来负向调节骨量，并且这些功能在卸载条件下增强。此外，利用微阵列技术对Runx2转基因小鼠骨细胞表达基因进行分析发现，在卸载条件下，5322个基因发生了变化（Dev Biol. 2006 Aug 1; 296(1): 48-61）。我们的发现将为理解骨细胞网络提供基础，骨细胞网络在骨量的调节中起着重要作用。

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.