Naslov
Cholesterol efflux mechanisms in endothelial cells of the human placenta

Autori
Panzenboeck, U. ; Štefulj, Jasminka ; Schweinzer, C. ; Desoye, G. ; Wadsack, C.

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
Journal of Clinical Lipidology / Brown, Virgil - New York (NY) : Elsevier, 2007, 356-356

Skup
XVI International Symposium on drugs affecting lipid metabolism

Mjesto i datum
Sjedinjene Američke Države, 04.10.2007. - 07.10.2007

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
cholesterol ; placenta ; LXR

Sažetak
Cholesterol is essential for normal fetal development. At the end of gestation, a considerable proportion of the fetal cholesterol demand is synthesized in fetal organs. However, fetuses with defects in endogenous cholesterol synthesis exhibit no birth defects, demonstrate the existence of external cholesterol sources. Maternal-fetal cholesterol transfer across the placenta is also supported by significantly higher levels of HDL-, LDL- and total cholesterol in umbilical venous than umbilical arterial plasma. It was estimated that up to 40% of the serum cholesterol in the term fetus may originate from maternal sources by transfer across the placenta. To travers this physical barrier between the maternal and fetal circulation, maternal cholesterol must be taken up on the maternal, apical side of the syncytiotrophoblast layer, released at the basolateral side, and subsequently traverse the fetal endothelial cell layer of the placenta, whose apical surface directly connects to the fetal circulation. In the present in vitro study we have analysed the final step in this proposed pathway of transplacental transfer of (lipoprotein) cholesterol – the efflux of cholesterol from fetal endothelial cells (FECs) of placenta. Using recently established method, arterial and venous primary FECs from human placenta were separately isolated, characterized and cultured as monolayers. The capacity of FECs to efflux cholesterol to either HDL3 or lipid-free apoA-I was tested using [³ ; ; H]-cholesterol labeled FECs. Significant time- and dose-dependent cholesterol efflux to both acceptors was observed. Induction of cholesterol efflux upon oxysterol treatment (to either or both apoA-I and HDL3) suggested the involvement of LXR- regulated lipid transporters, ABCA1, ABCG1 and/or ABCG4. In line, oxysterol-inducible cholesterol efflux was reflected by up- regulated mRNA and protein expression levels of ABCA1 and ABCG1 detected in FECs pre-treated with LXR agonists. Our data suggest that the apoA-I/ABCA1 and the HDL3/ABCG1 cholesterol efflux pathways are operative in FECs. In addition, a potential functional diversity of arterial and venous FECs in cholesterol release will be discussed.

Izvorni jezik
Engleski

Znanstvena područja
Biologija, Temeljne medicinske znanosti

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