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Interactive effects of PTH and mechanical stress on nitric oxide and PGE₂ production by primary mouse osteoblastic cells

Department of Oral Cell Biology, Academic Centre for Dentistry Amsterdam, Vrije Universiteit, NL-1081BT Amsterdam, The Netherlands

Submitted 14 November 2002 ; accepted in final form 9 May 2003

Parathyroid hormone (PTH) and mechanical stress both stimulate bone formation but have opposite effects on bone resorption. PTH increased loading-induced bone formation in a rat model, suggesting that there is an interaction of these stimuli, possibly at the cellular level. To investigate whether PTH can modulate mechanotransduction by bone cells, we examined the effect of 10^-9 M human PTH-(1-34) on fluid flow-induced prostaglandin E₂ (PGE₂) and nitric oxide (NO) production by primary mouse osteoblastic cells in vitro. Mechanical stress applied by means of a pulsating fluid flow (PFF; 0.6 ± 0.3 Pa at 5 Hz) stimulated both NO and PGE₂ production twofold. In the absence of stress, PTH also caused a twofold increase in PGE₂ production, but NO release was not affected and remained low. Simultaneous application of PFF and PTH nullified the stimulating effect of PFF on NO production, whereas PGE₂ production was again stimulated only twofold. Treatment with PTH alone reduced NO synthase (NOS) enzyme activity to undetectable levels. We speculate that PTH prevents stress-induced NO production via the inhibition of NOS, which will also inhibit the NO-mediated upregulation of PGE₂ by stress, leaving only the NO-independent PGE₂ upregulation by PTH. These results suggest that mechanical loading and PTH interact at the level of mechanotransduction.

parathyroid hormone; prostaglandin E₂; nitric oxide synthase

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