Increase in 15-hydroxyprostaglandin dehydrogenase activity in the ovine placentome at parturition and effect of oestrogen

Type 1 NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase (PGDH) is the key enzyme for metabolism of active primary prostaglandins to inactive for ms in gestational tissues. The present study examined the activity and immu nolocalization of PGDH in the ovine placenta, fetal membranes and uterus ov er the latter half of pregnancy, and its potential regulation by oestradiol . Placenta, fetal membranes and myometrium were collected from sheep with k nown single insemination dates on days 70, 100 and 135 of gestation and in active labour demonstrated by electromyographic activity. In addition, chro nically catheterized fetuses were infused with oestradiol (100 mu g kg(-1) per 24 h) (n = 5) or saline vehicle into the fetus from day 120 to day 125. PGDH activity measured in placental extracts remained constant from day 70 to day 135 of gestation, and then significantly (P < 0.05) increased by 30 0% in active labour. Immunoreactive PGDH was localized in the placentome at all stages and was present predominantly in the fetal component of the pla centome in uninucleate, but not in binucleate, trophoblast cells. Similarly , in the fetal membranes PGDH immunoreactivity was present in the uninuclea te trophoblast but not in the binucleate cells of the chorion. PGDH immunos taining was also present in the endometrial luminal epithelium, in the smoo th muscle of the myometrium, and the glandular epithelium of the cervix. In fusion of oestradiol into the fetal circulation from day 120 to day 125 of gestation had no effect on placental PGDH activity. Immunohistochemistry wa s used to localize oestrogen receptor a in intrauterine tissues to investig ate further the failure of oestradiol to increase PGDH activity. Immunoreac tive oestrogen receptor a was not present in the fetal component of the pla centa, although it was expressed in adjacent maternal-derived cells. It is concluded that (1) PGDH activity increases in late gestation; (2) PGDH is e xpressed in uninucleate trophoblast cells in the ovine placenta and fetal m embranes, and also in the maternal endometrial epithelium and stroma, myome trium and cervix; (3) oestrogen receptor a is not expressed in fetal cells in the placenta or fetal membranes; and (4) the increase in PGDH activity i s not regulated by oestradiol administered to the fetus.