| Autor: |
Suda, M., Tanaka, K., Sakuma, Y., Yasoda, A., Ozasa, A., Fukata, J., Tanaka, I., Narumiya, S., Nakao, K. |
| Předmět: |
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| Zdroj: |
Calcified Tissue International; Mar2000, Vol. 66 Issue 3, p217-223, 07p |
| Abstrakt: |
This study examined which subtype(s) of PGE receptors is involved in the induction of c-fos and c-jun by PGE2 in MC3T3-E1 cells. We also investigated the possibility that the induction of these genes is involved in the growth and differentiation of this cell line. PGE2 dose-dependently induced c-fos and c-jun mRNA expressions in MC3T3-E1 cells. Of the PGE analogs, 17-phenyl-ω-trinor PGE2 (EP1 agonist) and sulprostone (EP1/EP3 agonist) were far more potent than butaprost (EP2 agonist) and 11-deoxy PGE1 (EP2/EP4 agonist) in inducing c-fos and c-jun mRNA expressions. Since MC3T3-E1 cells do not express the EP3 subtype, these results suggest that PGE2 induces c-fos and c-jun mRNA expressions through the EP1 subtype of its receptor. In order to study the functional relevance of these protooncogenes, we then studied the effect of inhibition of their synthesis by the use of antisense oligonucleotide. Alkaline phosphatase (ALP) suppression by 17-phenyl-ω-trinor PGE2 was reversed by antisense oligonucleotide for either c-fos or c-jun. These results suggest that PGE2, via the EP1 subtype of the PGE receptor, negatively modulates the transition from proliferation to the matrix maturation stage through the induction of c-fos and c-jun. However, antisense oligonucleotide for c-fos or c-jun did not alter the prostaglandin G/H synthase-2 mRNA expression induced by EP1. Thus, it is possible that c-fos and c-jun inductions do not account for all the EP1-mediated PGE2 actions in MC3T3-E1 cells. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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