The Binding of High and Low Density Lipoproteins to Human Placental Membrane Fractions*

Cummings, Scott W.; Hatley, Warren; Simpson, Evan R.; Ohashi, Masao

doi:10.1210/jcem-54-5-903

Cited by 61 publications

(17 citation statements)

References 25 publications

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“…Tissues known to be rich in acid phosphatase, such as liver and kidney, have also been shown to take up apo A-I avidly [19,25]. It has also been demonstrated that HDL displays specific binding to placental cells [26] and testis membranes [27] but it is not known whether transfer of apo A-I to these cells occurs. Lysosomes play an important role in receptormediated endocytosis and catabolism of LDL [28].…”

Section: Discussionmentioning

confidence: 99%

Acid phosphatases bind to the main high density lipoprotein apolipoprotein A‐I

Vihko¹,

Wahlberg²,

Ehnholm³

et al. 1986

FEBS Letters

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The serum protein binding secretory prostatic acid phosphatase (PAP) and lysosomal placental acid phosphatase (LAP) was purified using affinity chromatography on gels containing immobilized acid phosphatases. The protein, which could be eluted from these enzyme affinity gels only with 0.05 HCl (pH 2.0), was shown to be apolipoprotein A‐I (apo A‐I), the main structural protein of high density lipoprotein (HDL).

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Section: Discussionmentioning

confidence: 99%

Acid phosphatases bind to the main high density lipoprotein apolipoprotein A‐I

Vihko¹,

Wahlberg²,

Ehnholm³

et al. 1986

FEBS Letters

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“…The human placental microvillous membrane contains specific binding sites for the lipoporoteins (VLDL, LDL and HDL), which transport TG and other esterified lipid (Cummings et al, 1982;Naoum et al, 1987;Wittmaack et al, 1995). The presence of lipoprotein lipase activity (Rothwell & Elphick, 1982;Shafrir & Barash, 1987;Kaminsky et al, 1991;Bonet et al, 1992) allows the production of NEFA from TG.…”

Section: Maternalmentioning

confidence: 99%

Effect of placental function on fatty acid requirements during pregnancy

Haggarty¹

2004

Eur J Clin Nutr

187

156

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The fetus has an absolute requirement for the n-3/n-6 fatty acids and docosahexaenoic acid (22:6 n-3; DHA) in particular is essential for the development of the brain and retina. Most of the fat deposition in the fetus occurs in the last 10 weeks of pregnancy. The likely rate of DHA utilisation during late pregnancy cannot be met from dietary sources alone in a significant proportion of mothers. De novo synthesis makes up some of the shortfall but the available evidence suggests that the maternal adipose tissue makes a significant contribution to placental transport to the fetus. The placenta plays a crucial role in mobilising the maternal adipose tissue and actively concentrating and channelling the important n-3/n-6 fatty acids to the fetus via multiple mechanisms including selective uptake by the syncytiotrophoblast, intracellular metabolic channelling, and selective export to the fetal circulation. These mechanisms protect the fetus against low long-chain polyunsaturated fatty acid (LCPUFA) intakes in the last trimester of pregnancy and have the effect of reducing the maternal dietary requirement for preformed DHA at this time. As a result of these adaptations, small changes in the composition of the habitual maternal diet before pregnancy are likely to be more effective in improving LCPUFA delivery to the fetus than large dietary changes in late pregnancy. There is little evidence that DHA intake/status in the second half of pregnancy affects visual and cognitive function in the offspring, but more studies are needed, particularly in children born to vegetarian and vegan and mothers who may have very low intakes of DHA.

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“…The fact that the placenta binds and internalizes maternal lipoproteins both in vivo and in vitro [8] suggests the existence of functionally intact lipoprotein receptors [2][3][4][5][6][7][8][9][10][11]. The presence of active lipoprotein receptors in the yolk sac, the placenta and placenta-derived cells support internalization of cholesterol-rich maternal lipoproteins [8].…”

mentioning

confidence: 99%

Trophoblast‐like human choriocarcinoma cells serve as a suitable in vitro model for selective cholesteryl ester uptake from high density lipoproteins

Wadsack¹,

Hrzenjak²,

Hammer³

et al. 2003

European Journal of Biochemistry

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As human choriocarcinoma cells display many of the biochemical and morphological characteristics reported for in utero invasive trophoblast cells we have studied cholesterol supply from high density lipoproteins (HDL) to these cells. Binding properties of 125I‐labeled HDL subclass 3 (HDL3) at 4 °C were similar for BeWo, JAr, and Jeg3 choriocarcinoma cell lines while degradation rates at 37 °C were highest for BeWo. Calculating the selective cholesteryl ester (CE)‐uptake as the difference between specific cell association of [3H]CE‐labeled HDL3 and holoparticle association of 125I‐labeled HDL3 revealed that in BeWo cells, the selective CE‐uptake was slightly lower than holoparticle association. However, the pronounced capacity for specific cell association of [3H]CE‐HDL3 and selective [3H]CE‐uptake in excess of HDL3–holoparticle association, and cAMP–mediated enhanced cell association of [3H]CE‐HDL3 in JAr and Jeg3 suggested the scavenger receptor class B, type I (SR‐BI) to be responsible for this pathway. Abundant expression of SR‐BI (but not SR‐BII, a splice variant of SR‐BI) could be observed in JAr and Jeg3 but not in BeWo cells using RT‐PCR, Northern and Western blot analysis, and immunocytochemical technique. Adenovirus‐mediated overexpression of SR‐BI in all three choriocarcinoma cell lines resulted in an enhanced capacity for cell association of [3H]CE‐HDL3 (20‐fold in BeWo; fivefold in JAr and Jeg3). The fact that exogenous HDL3 remarkably increases proliferation in JAr and Jeg3 supports the notion that selective CE‐uptake and subsequent intracellular generation of cholesterol is coupled to cellular growth. From our findings we propose that JAr and Jeg3 cells serve as a suitable in vitro model to study selective CE‐supply to human placental cells.

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The Binding of High and Low Density Lipoproteins to Human Placental Membrane Fractions*

Cited by 61 publications

References 25 publications

Acid phosphatases bind to the main high density lipoprotein apolipoprotein A‐I

Acid phosphatases bind to the main high density lipoprotein apolipoprotein A‐I

Effect of placental function on fatty acid requirements during pregnancy

Trophoblast‐like human choriocarcinoma cells serve as a suitable in vitro model for selective cholesteryl ester uptake from high density lipoproteins

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