Qiao Ju, Chen Weihui, Tian Weidong, Li Shengwei, Luo Songjiao
West China College of Stomatology, Sichuan University, Chengdu 610041, China.
Sheng Wu Yi Xue Gong Cheng Xue Za Zhi. 2004 Aug;21(4):575-8.
This study sought to elucidate the function of NO during the signal transduction wherein fluid shear stress regulates the proliferation and differentiation of osteoblast cells. The isolated rat osteoblast-like cells were exposed to fluid shear stress 12 dyn/cm2 for 5, 10, 15, 30, 60 and 120 min respectively with the use of a flow chamber. The NO release was examined. After the exposure to fluid shear stress, the NO synthesis of rat primary osteoblast-like cells increased significantly (P<0.05) when compared with the control. After 60 minutes of exposure, the release of NO began to increase significantly (P<0.05), but no significant increase as such was seen in the control (P>0.05). NO synthesis may be one of the signal transduction pathways which transduce the fluid shear stress into osteoblast cells. In early stage, it may be induced by cNOS and in late stage by iNOS.
本研究旨在阐明一氧化氮(NO)在流体剪切应力调节成骨细胞增殖和分化的信号转导过程中的作用。使用流动腔将分离的大鼠成骨样细胞分别暴露于12达因/平方厘米的流体剪切应力下5、10、15、30、60和120分钟,检测NO释放情况。暴露于流体剪切应力后,与对照组相比,大鼠原代成骨样细胞的NO合成显著增加(P<0.05)。暴露60分钟后,NO释放开始显著增加(P<0.05),但对照组未见显著增加(P>0.05)。NO合成可能是将流体剪切应力转导至成骨细胞的信号转导途径之一。早期可能由组成型一氧化氮合酶(cNOS)诱导,晚期由诱导型一氧化氮合酶(iNOS)诱导。