Periconceptional alcohol exposure impacts on placental structure and gene expression

37th Congress of IUPS (Birmingham, UK) (2013) Proc 37th IUPS, PCB343

Poster Communications: Periconceptional alcohol exposure impacts on placental structure and gene expression

E. M. Gardebjer1, J. Cuffe1, K. Moritz1

1. School of biomedical sciences, The university of queensland, Brisbane, Queensland, Australia.

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Perturbations during the periconceptional (PC) period are important determinants of a healthy pregnancy and offspring health. This period however is prior to maternal recognition of pregnancy when alcohol consumption is often a common social practice. Alcohol during pregnancy is known to impair the normal development of many organs and systems including the placenta. It is not known however whether alcohol consumption prior to implantation can impact on post implantation placental outcomes. This study aimed to examine if there were changes in the late gestation placenta (E20), of fetuses exposed to moderate levels of ethanol (EtOH) prior to implantation. Sprague-Dawley rats were exposed to a control liquid diet or one containing EtOH (12.5%, n=12/group) during the PC period (from embryonic day (E)-4 to E4). On E20, pregnant dams were deeply anesthetized with ketamine:xylazine (50:50) to ensure blood flow to fetuses and placentas during collection. Placentas from male and female fetuses were either fixed (whole) or frozen (as labyrinth and junctional zone separately). Dry weights of the placental components were derived by oven drying. Cross sectional areas of the labyrinth and junctional zone was determined following haemotoxylin/eosin staining. Relative mRNA expression of glucose transporters (GLUT1, GLUT3) and insulin like growth factors (IGF1 and IGF2) was examined via real-time PCR. Maternal plasma alcohol concentration reached an average maximum of 0.17%. There was no difference between groups in calorie intake but fetuses were growth restricted (p<0.05). Placental dry weight was significantly increased in EtOH-exposed fetuses (p=0.01) when normalized to body weight. This was due to an absolute (p=0.002) and normalized (p<0.0001) increase in weight of the junctional zone only. This was supported by an increase in the cross sectional area of the junctional zone in PC-EtOH exposed placentas (p=0.03) whilst the cross sectional area of the labyrinth zone was significantly smaller (p=0.03). While gene expression studies for GLUT1 and GLUT3 showed no difference in the labyrinth zone, GLUT3 was expressed at higher levels in the junctional zone of the placenta from PC-EtOH exposed females (p=0.03). IGF1 relative gene expression was reduced in the labyrinth of PC-EtOH exposed placentas (p=0.005) whereas the expression of IGF2 was unaffected. In contrast, whilst IGF2 expression was upregulated in the junctional zone (p=0.05), there was no difference observed for IGF1 expression in this zone. This study demonstrates that PC-EtOH significantly alters expression of key placental nutrient transporters and growth factors which are important for fetal growth and development. Moreover it also showed that exposure to EtOH prior to implantation alters the structure of the placenta and therefore potentially the future health of the offspring.



Where applicable, experiments conform with Society ethical requirements.

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