Zhuang H, Wang W, Tahernia A D, Levitz C L, Luchetti W T, Brighton C T
Department of Orthopaedic Surgery, University of Pennsylvania School of Medicine, Philadelphia 19082-6081, USA.
Biochem Biophys Res Commun. 1996 Dec 13;229(2):449-53. doi: 10.1006/bbrc.1996.1824.
It is well known that mechanical stimulation can prompt healing of bone fractures. However, the mechanism involved is less clear. In this study, we found that a 0.17% cyclic, biaxial mechanical strain delivered at 1 Hz increased proliferation of MC3T3-E1 cells, a clonal osteoblastic cell line. Mechanical strain also increased the level of TGF-beta 1 mRNA determined by quantitative reverse transcription/ polymerase chain reaction. Previous reports have shown that neomycin and W-7, which are inhibitors in the inositol phosphate/calmodulin pathway, blocked mechanical strain-induced proliferation of the osteoblast cells. Interestingly, we found that neomycin and W-7 can also block mechanical stimulation-induced elevation of TGF-beta 1 mRNA. Finally, using an antibody which blocked the action of TGF-beta 1, we found that the increased MC3T3-E1 cell proliferation induced by mechanical strain did not depend on the action of TGF-beta 1.
众所周知，机械刺激可促进骨折愈合。然而，其中涉及的机制尚不清楚。在本研究中，我们发现以1Hz施加的0.17%周期性双轴机械应变可增加MC3T3-E1细胞（一种克隆性成骨细胞系）的增殖。机械应变还增加了通过定量逆转录/聚合酶链反应测定的TGF-β1 mRNA水平。先前的报道表明，新霉素和W-7是肌醇磷酸/钙调蛋白途径中的抑制剂，可阻断机械应变诱导的成骨细胞增殖。有趣的是，我们发现新霉素和W-7也可阻断机械刺激诱导的TGF-β1 mRNA升高。最后，使用一种阻断TGF-β1作用的抗体，我们发现机械应变诱导的MC3T3-E1细胞增殖增加并不依赖于TGF-β1的作用。
