Maternal betamethasone administration reduces binucleate cell number and placental lactogen in sheep


Braun, Thorsten, Li, Shaofu, Moss, Timothy J.M., Newnham, John P., Challis, John R.G., Gluckman, Peter D. and Sloboda, Deborah M. (2007) Maternal betamethasone administration reduces binucleate cell number and placental lactogen in sheep. Journal of Endocrinology, 194, (2), 337-347. (doi:10.1677/JOE-07-0123).

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Original Publication URL: http://dx.doi.org/10.1677/JOE-07-0123

Description/Abstract

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.

Item Type: Article
ISSNs: 0022-0795 (print)
Related URLs:
Subjects: R Medicine > RC Internal medicine
Q Science > QH Natural history > QH301 Biology
Divisions: University Structure - Pre August 2011 > School of Medicine > Developmental Origins of Health and Disease
ePrint ID: 60933
Date Deposited: 24 Sep 2008
Last Modified: 27 Mar 2014 18:43
URI: http://eprints.soton.ac.uk/id/eprint/60933

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