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Research Communications |
Laboratory of Cell Growth, Department of Medicine, Veterans Affairs Medical Center, San Francisco, California 94121, USA
In serum-deprived MC3T3-E1 osteoblasts, mechanical stimulation caused by mild (287 x g) centrifugation induced a 10-fold increase in mRNA levels of the proto-oncogene, c-fos. Induction of c-fos was abolished by the cAMP-dependent protein kinase inhibitor H-89, suggesting that the transient c-fos mRNA increase is mediated by cAMP. Down-regulation of protein kinase C (PKC) activity by chronic TPA treatment failed to significantly reduce c-fos induction, suggesting that TPA-sensitive isoforms of PKC are not responsible for c-fos up-regulation. In addition, 287 x g centrifugation increased intracellular prostaglandin E2 (PGE2) levels 2.8-fold (P<0.005). Since we have previously shown that prostaglandin E2 (PGE2) can induce c-fos expression via a cAMP-mediated mechanism, we asked whether the increase in c-fos mRNA was due to centrifugation-induced PGE2 release. Pretreatment with the cyclooxygenase inhibitors indomethacin and flurbiprofen did not hinder the early induction of c-fos by mechanical stimulation. We conclude that c-fos expression induced by mild mechanical loading is dependent primarily on cAMP, not PKC, and initial induction of c-fos is not necessarily dependent on the action of newly synthesized PGE2.—Fitzgerald, J., Hughes-Fulford, M. Mechanically induced c-fos expression is mediated by cAMP in MC3T3-E1 osteoblasts.
1 Correspondence: Laboratory of Cell Growth, Department of Medicine, Veterans Affairs Medical Center, Mail code 151F, 4150 Clement St., San Francisco, CA, 94121, USA. E-mail: milliehf{at}aol.com
2 Current address: Orthopaedic Molecular Biology Research Unit, Department of Paediatrics, University of Melbourne, Royal Children's Hospital, Parkville, Victoria, 3052, Australia.
Key Words: gene expression • signal transduction • gravity • mechanical stimulation • PGE2 synthesis
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