Key result
ApoE-rHDL regulates ~1,400 genes in placental endothelial cells vs. 79 with fetal HDL.
Why the study?
Little is known about the role of fetal lipoproteins, specifically fetal HDL characterized by high apoE, in regulating gene expression in human placental endothelial cells.
Does fetal HDL or apoE-rHDL regulate gene expression in human placental endothelial cells?
Does fetal HDL or apoE-rHDL regulate gene expression in human placental endothelial cells?
Fetal HDL and apoE-rHDL regulate gene expression in human placental endothelial cells, particularly genes involved in cholesterol biosynthesis, cell protection, and metallothioneins.
ApoE-rHDL may broadly alter placental endothelial transcription versus fetal HDL; leaves open any role in fetal development pending in vivo confirmation.
Maternal lipoproteins have been studied extensively in human pregnancies, but little is known about the role of fetal lipoproteins. The vascularized human placenta interfaces between the mother and fetus to transfer nutrients for sustaining pregnancy. Unlike that of adults, fetal high-density lipoprotein (HDL), which is in contact with placental vessels, is characterized by a high proportion of apolipoprotein E (apoE). We hypothesize this unique composition of fetal HDL affects key functions of the growing fetal tissues. The aim was to identify genes regulated by apoE-HDL by incubating human placental endothelial cells (HPEC) with either fetal HDL or apoE-rich reconstituted HDL particles (apoE-rHDL). HPEC were exposed to 15 μg/ml fetal HDL, 15 μg/ml apoE-rHDL, or medium for 16 h, respectively. Microarray analysis determined genes regulated by fetal HDL and apoE. Characterization of HDL particles revealed a different hydrodynamic radius for apoE-rHDL (13.70 nm) compared with fetal HDL (18.11 nm). Stepwise gene clustering after microarray experiments identified 79 differentially expressed genes (P < 0.05) when cells were exposed to HDL compared with controls. Among them 16 genes were downregulated, whereas five genes were upregulated by twofold, respectively. When HPEC were incubated with apoE-rHDL 18-fold more genes (1,417, 12% of transcripts) were regulated (P < 0.05) in contrast to HDL. Thereof, 172 genes were downregulated and 376 genes upregulated (twofold). In the common subset of 38 genes regulated by both HDL particles, genes involved in cholesterol biosynthesis and cell protection prevailed. Strikingly, results suggest that HDL has the capability of regulating metallothioneins, which may have an effect on oxidative stress in HPEC.
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Augsten et al. (2011) studied Human placental endothelial cells (in vitro). Fetal HDL and apoE-rich reconstituted HDL particles (apoE-rHDL) vs. Medium (controls) was evaluated on Differentially expressed genes (p=<0.05). Incubation of human placental endothelial cells with apoE-rHDL regulated 1,417 genes compared to 79 genes regulated by fetal HDL (P<0.05), including genes for cholesterol biosynthesis and cell protection.
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