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Prostacyclin (PGI 2 ): a potential mediator of c‐fos expression induced by hydrostatic pressure in osteoblastic cells
Author(s) -
GLANTSCHNIG H.,
VARGA F.,
RUMPLER M.,
KLAUSHOFER K.
Publication year - 1996
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.1996.165312.x
Subject(s) - prostacyclin , activator (genetics) , hydrostatic pressure , chemistry , prostaglandin , medicine , endocrinology , messenger rna , prostaglandin e2 , microbiology and biotechnology , biology , biochemistry , receptor , gene , physics , thermodynamics
Application of compressive forces to osteoblastic cells is known to cause specific cellular responses. We report that hydrostatic pressure increased c‐ fos mRNA expression in MC3T3‐E1 cells after 15, 30 and 60min. This effect was absent when 5×10 −7 molL −1 indomethacin, an inhibitor of prostaglandin synthesis, was present in the culture medium during pressurization. Using radioimmunoassays, a significant increase in the concentrations of 6‐keto‐PGF 1α , the stable conversion product of prostacyclin (PGI 2 ), in the conditioned medium of pressurized cells, was measured after 60min. In contrast, PGE 2 levels were not significantly changed and we therefore assume that under these experimental conditions PGE 2 is not responsible for the transduction of the hydrostatic force. However, we also found that PGE 2 has the capacity to induce c‐ fos mRNA in MC3T3‐E1 cells. Furthermore, we show for the first time that the stable prostacyclin analogue, Iloprost‐Trometamol (Ilomedin), is a potent activator of c‐ fos gene transcription. Our data suggest that prostacyclin is a likely candidate in mediating the effect of hydrostatic compressive stress on bone cells by regulating the level of c‐ fos mRNA, a member of the activator protein (AP)‐1 complex and potent regulator of osteoblastic proliferation and differentiation.