Hillsley M V, Frangos J A
Department of Chemical Engineering, Pennsylvania State University, University Park, USA.
J Bone Miner Res. 1996 Jan;11(1):114-24. doi: 10.1002/jbmr.5650110116.
It is our hypothesis that osteoblasts play a major role in regulating bone (re)modeling by regulating interstitial fluid (ISF) flow through individual bone compartments. We hypothesize that osteoblasts of the blood-bone membrane lining the bone surfaces are capable of regulating transosseous fluid flow. This regulatory function of the osteoblasts was tested in vitro by culturing a layer of rat calvarial osteoblasts on porous membranes. Such a layer of osteoblasts subjected to 7.3 mm Hg of hydrostatic pressure posed a significant resistance to fluid flow across the cell layer similar in magnitude to the resistance posed by endothelial monolayers in vitro. The hydraulic conductivity, the volumetric fluid flux per unit pressure drop, of the osteoblast layer was altered in response to certain hormones. Hydraulic conductivity decreased approximately 40% in response to 33 nM parathyroid hormone, while it exhibited biphasic behavior in response to calcitonin: increased 40% in response to 100 nM calcitonin and decreased 40% in response to 1000 nM calcitonin. Further, activation of adenylate cyclase by forskolin dramatically increased the hydraulic conductivity, while elevation of intracellular calcium, [Ca2+]i, by the calcium ionophore A23187 initially decreased the hydraulic conductivity at 5 minutes before increasing conductivity by 30 minutes. These results suggest that cyclic adenosine monophosphate (cAMP) and [Ca2+]i may mediate changes in the osteoblast hydraulic conductivity. The increase in hydraulic conductivity in response to 100 nM calcitonin and the decrease in response to PTH suggest that the stimulatory and inhibitory effects on bone formation of calcitonin and parathyroid hormone, respectively, may be due in part to alterations in bone fluid flow.
我们的假设是，成骨细胞通过调节穿过各个骨腔室的组织液（ISF）流动，在调节骨（再）建模中起主要作用。我们假设，衬于骨表面的血-骨膜中的成骨细胞能够调节经骨的液体流动。通过在多孔膜上培养一层大鼠颅骨成骨细胞，在体外对成骨细胞的这种调节功能进行了测试。这样一层承受7.3毫米汞柱静水压力的成骨细胞对穿过细胞层的液体流动产生了显著阻力，其大小与体外内皮单层细胞产生的阻力相似。成骨细胞层的水力传导率（单位压力降的体积液体通量）会因某些激素而改变。响应33 nM甲状旁腺激素时，水力传导率降低约40%，而响应降钙素时则表现出双相行为：响应100 nM降钙素时增加40%，响应1000 nM降钙素时降低40%。此外，福斯可林激活腺苷酸环化酶会显著增加水力传导率，而钙离子载体A23187使细胞内钙浓度[Ca2+]i升高时，最初在5分钟时会降低水力传导率，30分钟后传导率增加。这些结果表明，环磷酸腺苷（cAMP）和[Ca2+]i可能介导成骨细胞水力传导率的变化。响应100 nM降钙素时水力传导率增加，响应甲状旁腺激素时降低，这表明降钙素和甲状旁腺激素对骨形成的刺激和抑制作用，可能部分归因于骨液流动的改变。
