Abstract
High levels of atherogenic lipids in pregnancy are associated with health complications for the mother, the fetus and the newborn. As endocrine secretory tissue, the human placenta releases apolipoproteins (apos), particularly apoA1 and apoE. However, the magnitude and the directionality of the apo secretions remain unknown. We aimed to 1) determine the amount and orientation (apical-maternal versus basal-fetal) of placentally secreted apoA1 and apoE using human perfused placenta and primary trophoblast cell (PTC) culture, 2) compare apoA1 and apoE secretions of PTC with that of hepatocytes and 3) associate the obtained results with human blood levels by determining apoA1 and apoE concentrations in maternal and fetal serum samples. In perfused placenta and serum samples, apoA1 and apoE concentrations were significantly higher at the maternal compared to the fetal side. For apoE a similar trend was found in PTC. For apoA1, the secretion to the apical side declined over time while release to the basal side was stable resulting in significantly different apoA1 concentrations between both sides. Unexpectedly, PTC secreted significantly higher amounts of apoA1 and apoE compared to hepatocytes. Our data indicate that the placenta may play an important role in maternal and fetal cholesterol homeostasis via secretion of anti-atherogenic apos.
Highlights
Fetal development and growth depend on appropriate in utero homeostasis, which is regulated by placental transport and metabolism of maternal nutrients into the fetal circulation[1]
In order to validate our findings from the placenta perfusion in an additional physiological system, we investigated the magnitude and directionality of apoA1 and apoE secretion in primary trophoblast cells grown as monolayers on Transwell filter supports
We determined for the first time the magnitude as well as the directionality of placental apoA1 and apoE secretion in two highly physiological human placenta models
Summary
Fetal development and growth depend on appropriate in utero homeostasis, which is regulated by placental transport and metabolism of maternal nutrients into the fetal circulation[1]. A dysregulation in the placental transport of nutrients is an important risk factor for complications during perinatal development that can extend into adult life[2,3] In this context, cholesterol plays an important role as nutrient required for normal fetal development. Pregnancy is a proatherogenic-like physiological state, which is accompanied by substantial dyslipidemia in second and third trimester[14,15] Pathologies such as preeclampsia, a human pregnancy-related disease, impair maternal vascular functions and compromise fetal development. The quantitative capacity of the placenta to synthesize, store and release apos has not been determined These aspects, are fundamental as apos could have a major impact on the mother’s lipid profile during pregnancy and could play a supportive role in regulating maternal and fetal cholesterol homeostasis
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