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1 Department of Physiology and Obstetrics and Gynecology, University of Toronto, MSB, Room 3344, 1 King’s College Circle, Toronto, Ontario, Canada M5S 1A1
2 Department of Obstetrics and Gynecology, Heinrich Heine University Düsseldorf, Moorenstr. 5, 40225 Düsseldorf, Germany
3 School of Women’s and Infants’ Health, King Edward Memorial Hospital, The University of Western Australia, 374 Bagot Road, Subiaco 6008, Western Australia
4 Women and Infants Research Foundation, King Edward Memorial Hospital, The University of Western Australia, 374 Bagot Road, Subiaco 6008, Western Australia
5 The Liggins Institute, University of Auckland, Private Bag 92019, Auckland, New Zealand
(Correspondence should be addressed to J R G Challis; Email: j.challis{at}utoronto.ca)
The placenta may mediate glucocorticoid-induced fetal growth restriction. Previous studies have examined effects of fetal cortisol in sheep, which reduces placental binucleate cell (BNC) number; the source of ovine placental lactogen (oPL). The effects of maternal GC are unknown. Therefore, this study examined the effects of maternal betamethasone (BET) administration on BNC number, distribution, placental oPL protein levels, and maternal and fetal plasma oPL levels. Pregnant ewes were randomized to receive injections of saline or one (104 days of gestation; dG), two (104 and 111 dG), or three (104, 111, and 118 dG) doses of BET (0.5 mg/kg). Placental tissue was collected before, during, and after the period of BET treatment. Fetal (121–146 dG) and placental (121 dG) weights were decreased after BET when compared with controls. In controls, the mean number of BNCs increased until 132 dG and decreased thereafter. Placental oPL protein levels peaked at 109 dG and remained stable thereafter. Maternal plasma oPL levels in controls increased across gestation; fetal plasma oPL levels decreased. BNCs were reduced by 24% to 47% after BET when compared with controls at all ages studied. Placental oPL protein levels, maternal, and fetal plasma oPL levels were also reduced after BET injections, but recovered to values that were not different to controls near term. BET disrupted the normal distribution of BNCs within the placentome. These data may suggest a placental role in growth restrictive effects of prenatal maternal BET exposure through alterations in placental output of oPL, a key metabolic hormone of pregnancy.
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