Osteoblasts respond to pulsatile fluid flow with shortterm increases in PGE2 but no change in mineralization

被引:86
作者
Nauman, EA
Satcher, RL
Keaveny, TM
Halloran, BP
Bikle, DD
机构
[1] Univ Calif Berkeley, Dept Mech Engn, Orthopaed Biomech Lab, Berkeley, CA 94720 USA
[2] Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA
[3] Univ Calif San Francisco, Dept Orthopaed Surg, San Francisco, CA 94143 USA
[4] Univ Calif San Francisco, Vet Affairs Med Ctr, San Francisco, CA 94143 USA
关键词
bone remodeling; parallel-plate flow chamber; tissue engineering;
D O I
10.1152/jappl.2001.90.5.1849
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Although there is no consensus as to the precise nature of the mechanostimulatory signals imparted to the bone cells during remodeling, it has been postulated that deformation-induced fluid flow plays a role in the mechanotransduction pathway. In vitro, osteoblasts respond to fluid shear stress with an increase in PGE(2) production; however, the long-term effects of fluid shear stress on cell proliferation and differentiation have not been examined. The goal of this study was to apply continuous pulsatile fluid shear stresses to osteoblasts and determine whether the initial production of PGE(2) is associated with long-term biochemical changes. The acute response of bone cells to a pulsatile fluid shear stress (0.6 +/- 0.5 Pa, 3.0 Hz) was characterized by a transient fourfold increase in PGE(2) production. After 7 days of static culture (0 dyn/cm(2)) or low (0.06 +/- 0.05 Pa, 0.3 Hz) or high (0.6 +/- 0.5 Pa, 3.0 Hz) levels of pulsatile fluid shear stress, the bone cells responded with an 83% average increase in cell number, but no statistical difference (P > 0.53) between the groups was observed. Alkaline phosphatase activity per cell decreased in the static cultures but not in the low- or high-flow groups. Mineralization was also unaffected by the different levels of applied shear stress. Our results indicate that short-term changes in PGE(2) levels caused by pulsatile fluid flow are not associated with long-term changes in proliferation or mineralization of bone cells.
引用
收藏
页码:1849 / 1854
页数:6
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