Abstract
We have reported previously that PGE2 evoked an increase in intracellular calcium level ( [Ca2+] i) in mouse osteoblastic cells (Eicosanoids, 3, 157-160) . Here, we investigated the effects of PGE1 and PGF2a on cAMP production and [Ca2+] i in comparison with those of PGE2. In osteoblastic clone, MC3T3-E1 cells, PGE1 stimulated cAMP production, but has no effect on [Ca2+] i whereas PGF2a evoked only [Ca2+] i increase. In contrast, PGE2 not only stimulated cAMP production, but also increased [Ca2+] i. From the Scatchard plot analysis of PGE2 it is confirmed that there are two classes of PGE2 binding sites (Kd value, 9.2 nM; binding site, 29 fmole/mg protein, and Kd value, 134 nM; binding site, 148 fmole/mg protein) .These data indicate the possibility that the dual action of PGE2 is mediated by distinct receptor systems. As increase in [Ca2+] i was caused by PGF2a and PGE2, but not by PGE1, we investigated the displacement study of [3H] -PGF2a binding. The displacement capacity of unlabeled PGE2 was about 1/10 of that of PGF2a, while that of PGE1 was very low even at 500-fold excess.These data suggest that the dual effect of PGE2 is mediated by distinct receptor systems.
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