Transport of maternal LDL and HDL to the fetal membranes and placenta of the Golden Syrian hamster is mediated by receptor-dependent and receptor-independent processes.

نویسندگان

  • K L Wyne
  • L A Woollett
چکیده

Maternal lipoproteins provide nutrients to the fetus via the placenta, yolk sac, and uterine membrane plus decidua. To determine the transport processes that are responsible for the removal of lipoproteins from the maternal circulation, we measured the clearance rates of maternal LDL and HDL in vivo, as well as the tissue distribution of expression of the LDL receptor, glycoprotein 330 (gp330) and the newly described HDL receptor, SR-BI, in the placenta, yolk sac, and uterine membrane plus decidua at mid- and late-gestation of the hamster. In mid-gestation (day 10.5), LDL clearance rates of the placenta and yolk sac were similar to those in the liver (approximately 100 microl/h per g) and higher than those in the decidua (18 +/- 3 microl/h per g). Clearance rates for HDL-apoA-I and HDL-cholesteryl ether were similar to those of LDL in the placenta and decidua whereas rates in the yolk sac were dramatically higher (>1700 microl/h per g). Additionally, albumin was cleared in the placenta and decidua at approximately 16 microl/h per g whereas the yolk sac cleared the protein at much higher rates (196 +/- 22 microl/h per g). Low levels of LDL receptor were detected by immunoblot analysis in the placenta with trace amounts in the yolk sac. Gp330 and SR-BI were both barely detectable in the placenta but were expressed at high levels in the yolk sac. As gestation progressed to day 14.5, LDL and HDL clearance rates decreased in all three tissues; immunodetectable LDL receptor decreased in the placenta whereas the expression of gp330 and SR-BI in the placenta and yolk sac remained relatively constant. These data suggest that the clearance of maternal lipoproteins by the placenta, yolk sac, and decidua are mediated by receptor-mediated as well as receptor-independent processes.

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عنوان ژورنال:
  • Journal of lipid research

دوره 39 3  شماره 

صفحات  -

تاریخ انتشار 1998