Review: The feto-placental unit, pregnancy pathology and impact on long term maternal health
The Robinson Institute, Obstetrics and Gynaecology, University of Adelaide, SA, Australia.Placenta (Impact Factor: 2.71). 11/2011; 33 Suppl(Suppl):S37-41. DOI: 10.1016/j.placenta.2011.11.005
Pregnancy induces a number of alterations to maternal physiology to accommodate the increased demands made by the developing fetus and placenta. These alterations appear at least in part to be driven by products derived from the feto-placental unit, including microchimeric cells, as well as placental exosomes and microparticles, inducing changes to maternal physiology both during pregnancy and beyond. Further, increasing evidence suggests that some of these alterations are dependent on the sex of the fetus. Pre-eclampsia and asthma represent two common pregnancy complications that have provided valuable insight into how the feto-placental unit influences maternal physiology in a sex-specific manner. Pregnancy-induced alterations in maternal physiology may expose pre-existing subclinical pathologies and provide insight into future maternal health and disease. While most pregnancy-induced alterations to the maternal system are reversed following delivery, some can persist after parturition leading to cardiovascular, metabolic and autoimmune disease and increased risk of early mortality.
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- "Pregnancy induces several placental-mediated hemodynamic adaptations of maternal physiology to deal with the increased demands of the developing fetal-placental unit. Placental gene expression is known to be fetal sex specific  . Furthermore, earlier studies showed that the fetoplacental unit influences maternal physiology in a sex specific manner with stronger expressions of placental cytokine mRNA among female placentas resulting in altered maternal asthma symptomatology between women carrying a female and women carrying a male fetus [3e5]. "
ABSTRACT: Evidence indicates a gender specific interaction between the mother, placenta and fetus in which maternal adaptation to pregnancy and outcome partly depends on fetal gender. This study assesses fetal gender specific differences in placental biomarkers and uteroplacental vascular resistance. Methods Within the Generation R Study, in 1st and 2nd trimester (median 13.3 and 20.4 wks) blood samples were drawn to assess soluble fms-like tyrosine kinase (s-Flt1), placental growth factor (PLGF) and plasminogen activator inhibitor 2 (PAI-2). Uteroplacental resistance was assessed by mean pulsatility index (PI) of the uterine and umbilical arteries in the 2nd trimester. Mann-Whitney U and Student's t-test were performed to assess associations of gender on the above mentioned factors. In total 8631 women were included (4274 female and 4357 male fetuses). From these women, 172 had a pregnancy complicated by pre-eclampsia (1.9%). Fetal sex related differences in placental biomarkers, being most pronounced in non pre-eclamptic pregnancies (Table 1). Differences were also observed between early (<34wks) and late onset pre-eclamptic women (>34wks). This study shows that maternal adaptation to pregnancy varies by fetal gender, suggesting gender specific differences in placentation and placental function. The differences between pre-eclamptic and non pre-eclamptic women, and among pre-eclamptic women, suggest that different mechanisms apply to pre-eclamptic pregnancies. Copyright © 2013. Published by Elsevier B.V.
- "The differences in risk among ethnic groups suggest a strong role for genetic factors in the pathogenesis of preeclampsia. Most theories on the etiology of preeclampsia suggest that the disease is a cascade triggered by combination of abnormal maternal inflammatory response, endothelial cell activation/damage with deranged hemodynamic milieu, and deranged immunity [7–12]. The precise trigger that unifies the deranged vascular, immune and inflammatory responses remains to be elucidated. "
Article: Preeclampsia 2012[Show abstract] [Hide abstract]
ABSTRACT: Preeclampsia is a common complication of pregnancy associated with high maternal morbidity and mortality and intrauterine fetal growth restriction. There is extensive evidence that the reduction of uteroplacental blood flow in this syndrome results from the toxic combination of hypoxia, imbalance of angiogenic and antiangiogenic factors, inflammation, and deranged immunity. Women treated for preeclampsia also have an increased risk for cardiovascular and renal disease. At present it is unclear if the increased cardiovascular and renal disease risks are due to residual and or progressive effects of endothelial damage from the preeclampsia or from shared risk factors between preeclampsia and cardiac disease. Moreover, it appears that endothelin-1 signaling may play a central role in the hypertension associated with preeclampsia. In this paper, we discuss emerging data on the pathogenesis of preeclampsia and review therapeutic options.
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ABSTRACT: Angiotensin II type I receptor agonistic autoantibodies (AT1-AA) are related to pre-eclampsia and hypertension and have a direct effect of stimulating the production of tumor necrosis factor-alpha (TNF-α) in the placenta. TNF-α is a known mediator of apoptosis. However, few studies have reported the role of TNF-α and its relationship within AT1-AA-induced apoptosis of cardiomyocytes. In this study, neonatal rat cardiomyocytes were treated with various concentrations of AT1-AA. The apoptosis of neonatal rat cardiomyocytes was determined using TUNEL assay and flow cytometry. The level of secreted TNF-α was measured by enzyme-linked immunosorbent assay, and caspase-3 activity was measured by a fluorogenic protease assay kit. AT1 receptor blockade and TNF inhibitor were added to determine whether they could inhibit the apoptotic effect of AT1-AA. Results showed that AT1-AA induced the apoptosis of neonatal rat cardiomyocytes in a dose-dependent and time-dependent manner. AT1-AA increased TNF secretion and caspase-3 activities. AT1 receptor blockade completely abrogated AT1-AA-induced TNF-α secretion, caspase-3 activation, and cardiomyocyte apoptosis. TNF-α receptor inhibitor significantly attenuated AT1-AA-induced neonatal rat cardiomyocyte apoptosis. AT1-AA in the plasma of pre-eclamptic patients promoted neonatal rat cardiomyocyte apoptosis through a TNF-caspase signaling pathway.
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