Presence of CLA-1 and HDL Binding Sites on Syncytiotrophoblast Brush Border and Basal Plasma Membranes of Human Placenta

Lafond, Julie; Charest, Marie-Claude; Alain, J.-F; Brissette, Louise; Masse, André; Robidoux, Jacques; Simoneau, Lucie

doi:10.1053/plac.1999.0412

Cited by 31 publications

(15 citation statements)

References 45 publications

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“…HDL serves as a physiological cholesterol/CE-carrier during reverse cholesterol transport from peripheral tissue to the liver and/or steroidogenic tissues. As HDL may exert biological action in human trophoblast cells [50] we have investigated binding, cell association, and holoparticle association of HDL 3 as well as selective CE-uptake from HDL 3 (Table 1) comparable to those when binding of HDL 3 to trophoblast membrane protein fractions [3,51] or to intact first trimester trophoblasts was investigated [52]. However, the pronounced capability for lipid tracer uptake from CE-labeled HDL 3 in excess of holoparticle association in JAr and Jeg3 (but not in BeWo) cells was indicative for SR-BI-mediated selective CE-uptake from HDL 3 in these cell lines.…”

Section: Discussionmentioning

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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Section: Discussionmentioning

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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“…296 and 297) as well as in basal plasma membrane (i.e., the side facing the developing fetus; Ref. 297). …”

Section: Embryonic and Extraembryonic Tissuesmentioning

confidence: 99%

The Role of the High-Density Lipoprotein Receptor SR-BI in the Lipid Metabolism of Endocrine and Other Tissues

2003

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Because cholesterol is a precursor for the synthesis of steroid hormones, steroidogenic tissues have evolved multiple pathways to ensure adequate supplies of cholesterol. These include synthesis, storage as cholesteryl esters, and import from lipoproteins. In addition to endocytosis via members of the low-density lipoprotein receptor superfamily, steroidogenic cells acquire cholesterol from lipoproteins by selective lipid uptake. This pathway, which does not involve lysosomal degradation of the lipoprotein, is mediated by the scavenger receptor class B type I (SR-BI). SR-BI is highly expressed in steroidogenic cells, where its expression is regulated by various trophic hormones, as well as in the liver. Studies of genetically manipulated strains of mice have established that SR-BI plays a key role in regulating lipoprotein metabolism and cholesterol transport to steroidogenic tissues and to the liver for biliary secretion. In addition, analysis of SR-BI-deficient mice has shown that SR-BI expression is important for alpha-tocopherol and nitric oxide metabolism, as well as normal red blood cell maturation and female fertility. These mouse models have also revealed that SR-BI can protect against atherosclerosis. If SR-BI plays similar physiological and pathophysiological roles in humans, it may be an attractive target for therapeutic intervention in cardiovascular and reproductive diseases.

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“…These cells take up LDL-CE via receptor-mediated and receptor-independent processes (45,58). In addition, BeWo cells express the LDL receptor and SR-BI, as do placental cells (75,76). However, these data are not in agreement with a recent study suggesting that BeWo cells do not express SR-BI (57).…”

Section: Discussionmentioning

confidence: 62%

Transport of cholesterol across a BeWo cell monolayer

Schmid

Davidson

Myatt

et al. 2003

Journal of Lipid Research

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The placental transport of various compounds, such as glucose and fatty acids, has been well studied. However, the transport of cholesterol, a sterol essential for proper fetal development, remains undefined in the placenta. Therefore, the purpose of these studies was to examine the transport of cholesterol across a placental monolayer and its uptake by various cholesterol acceptors. BeWo cells, which originated from a human choriocarcinoma, were grown on transwells for 3 days to form a confluent monolayer. The apical side of the cells was radiolabeled with either free cholesterol or LDL cholesteryl ester. After 24 h, the radiolabel was removed and cholesterol acceptors were added to the basolateral chamber. Cholesterol was found to be taken up by the apical surface of the placental monolayer, transported to the basolateral surface of the cell, and effluxed to fetal human serum, fetal HDL, or phospholipid vesicles, but not to apolipoprotein A-I. In addition, increasing the cellular cholesterol concentration further increased the amount of cholesterol transported to the basolateral acceptors. These are the first studies to demonstrate the movement of cholesterol across a placental cell from the maternal circulation (apical side) to the fetal circulation (basolateral side).

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Presence of CLA-1 and HDL Binding Sites on Syncytiotrophoblast Brush Border and Basal Plasma Membranes of Human Placenta

Cited by 31 publications

References 45 publications

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

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

The Role of the High-Density Lipoprotein Receptor SR-BI in the Lipid Metabolism of Endocrine and Other Tissues

Transport of cholesterol across a BeWo cell monolayer

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