Expression of prostanoid receptors in human lower segment pregnant myometrium

Andreas Leonhardt, Alexander P. Glaser, Markus Wegmann, Reinhard Hackenberg, Rolf M. Nüsing
In: Prostaglandins, Leukotrienes and Essential Fatty Acids · 2003 · vol. 69(5) , pp. 307–313 · doi:10.1016/s0952-3278(03)00113-3 · PMID:14580364 · W1992900172
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Human pregnant myometrium expresses mRNA and protein for EP1, EP2, EP3, EP4, FP, TP, and IP prostanoid receptors, with EP2 expression inversely related to gestational age.

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Abstract

Prostanoids, especially prostaglandin (PG) E(2), are important mediators of uterine relaxation and contractions during gestation and parturition. Inhibitors of PG formation as well as PG analogues are used to modulate uterine tonus. So far, only limited data are available regarding the expression of prostanoid receptors in human pregnant myometrium. In the present study, the expression of the receptors for PGE(2) (EP1, EP2, EP3, EP4), PGF(2alpha) (FP), prostacyclin (IP), and thromboxane A(2) (TP) in human pregnant myometrium was studied by RT-PCR, in situ hybridization and immunohistochemistry. Myometrial tissue was obtained from five women at term and not in labour and from two women who delivered preterm. Tissue specimens were excised from the upper edge of the transverse lower uterine segment incision. In all tissues analysed, EP1, EP2, EP3, EP4, FP, TP and IP receptor mRNA and protein was detected. mRNA expression for PGD(2) (DP) receptor was not detected in the majority of tissue specimens. EP1, EP2, EP4, IP, TP and FP receptor protein was detected on myometrial smooth muscle cells, whereas EP3 receptor protein was only expressed by stromal and endothelial cells. In situ hybridization experiments yielded similar results. The expression of the EP2 receptor mRNA was inversely related to gestational age. We suggest that the contractile effect of PGE(2) at term is probably mediated directly by the EP1 receptor expressed in myometrial smooth muscle cells and indirectly by the EP3 receptor expressed in stromal cells and a decrease in EP2 receptor expression.

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