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Articles in PresS, published online ahead of print April 23, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00547.2001
Submitted on December 12, 2001
Accepted on April 9, 2002
1 Bioengineering, University of California San Diego, La Jolla, CA, USA
* To whom correspondence should be addressed. E-mail: chazwhite{at}hotmail.com.
Bone cells are subject to interstitial fluid flow (IFF) driven by venous pressure and mechanical loading. Rapid dynamic changes in mechanical loading cause transient gradients in IFF. The effects of pulsatile flow (temporal gradients in fluid shear) on rat UMR106 cells, and rat primary osteoblastic cells were studied. Pulsatile flow induced a 95% increase in S phase UMR106 cells compared to static controls. In contrast, ramped steady flow stimulated only a 3% increase. Similar patterns of S phase induction were also observed in rat primary osteoblastic cells. Pulsatile flow significantly increased relative UMR106 cell number by 37% and 62% at 1.5 hr and 24 hrs (respectively). Pulsatile flow also significantly increased Erk1/2 phosphorylation by 418%, while ramped steady flow reduced Erk1/2 activation to 17% of control. Correspondingly, retinoblastoma protein was significantly phosphorylated by pulsatile fluid flow. Inhibition of MEK1/2 by U0126 (a specific MEK1/2 inhibitor) reduced shear-induced Erk1/2 phosphorylation, and cell proliferation. These findings suggest that temporal gradients in fluid shear stress are potent stimuli of bone cell proliferation.
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