Angiotensin II Promotes Selective Uptake of High Density Lipoprotein Cholesterol Esters in Bovine Adrenal Glomerulosa and Human Adrenocortical Carcinoma Cells Through Induction of Scavenger Receptor Class B Type I

Cherradi, Nadia

doi:10.1210/en.142.10.4540

Cited by 24 publications

(16 citation statements)

References 48 publications

(65 reference statements)

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“…The fact that BeWo, a cell line with many characteristics of cytotrophoblast, are almost lacking SR-BI and SR-BI-mediated selective CE-uptake from HDL 3 , supports the assumption that JAr and Jeg3 resembling syncytiotrophoblasts-like properties are suitable in vitro models to study directed cholesterol/CE-transport in polarized cells. Invasiveness of trophoblast cells in vivo and choriocarcinoma cells in vitro apparently is linked to celldifferentiation and proliferation [47] similar to that reported for other tumors [62,63].…”

Section: Discussionsupporting

confidence: 73%

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: Discussionsupporting

confidence: 73%

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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“…Lipoprotein receptor expression and AngII-mediated regulation of lipoprotein metabolism in H295R adrenocortical cells have been studied previously (Martin et al 1999, Cherradi et al 2001, Pilon et al 2003. Cherradi et al (2001) and Pilon et al (2003) reported that AngII stimulated SR-BI, but not LDL receptor expression.…”

Section: Discussionmentioning

confidence: 99%

“…Cherradi et al (2001) and Pilon et al (2003) reported that AngII stimulated SR-BI, but not LDL receptor expression. Recently, it has been shown that AngII induced uptake of LDL in primary human adrenocortical cells and stimulated aldosterone and cortisol synthesis (Liang et al 2007).…”

Section: Discussionmentioning

confidence: 99%

Prediabetic and diabetic in vivo modification of circulating low-density lipoprotein attenuates its stimulatory effect on adrenal aldosterone and cortisol secretion

Kopprasch¹,

Pietzsch²,

Ansurudeen³

et al. 2008

Journal of Endocrinology

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Modification of low-density lipoprotein (LDL) and abnormal aldosterone and cortisol metabolism have been implicated in the pathogenesis of type 2 diabetes (DM2) and diabetic vascular disease. Since LDL serves as a major cholesterol source for adrenal steroidogenesis, we investigated whether LDL modification in prediabetic and diabetic subjects influences adrenocortical aldosterone and cortisol release. LDL was isolated from 30 subjects with normal glucose tolerance (NGT-LDL), 30 subjects with impaired glucose tolerance (IGT-LDL), and 26 patients with DM2 (DM2-LDL). Oxidation and glycoxidation characteristics of LDL apolipoprotein B100 of each individual was assessed by gas chromatography-mass spectrometry analysis. Human adrenocortical cells (NCI-H295R) were incubated for 24 h with 100 mg/ml LDL and after removal of supernatants stimulated for a further 24 h with angiotensin II (AngII). In supernatants, aldosterone and cortisol secretion was measured. IGT-LDL and DM2-LDL were substantially more modified than NGT-LDL. Each of the five measured oxidation/glycoxidation markers was significantly positively associated with glycemic control, measured as HbA 1c . LDL from all subjects stimulated both the basal and AngII-induced aldosterone and cortisol release from adrenocortical cells. However, hormone secretion was significantly inversely related to the degree of LDL oxidation/glycoxidation. We conclude that LDL modifications in IGT and DM2 subjects may have significant clinical benefits by counteracting prediabetic and diabetic overactivity of the renin-angiotensinaldosterone system and enhanced cortisol generation.

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“…This translocation process is rapid and implicates a mobilization of intracellular pools, as no significant increase in SR-B1 protein level was observed. This short term regulatory effect seems to be specific to 3T3L1 and primary adipocytes because, in other cell types such as the adrenal gland and the gonads, trophic hormones were reported to stimulate SRB1 expression after 24 h. This was associated with enhanced uptake of HDL-delivered cholesterol esters and steroidogenesis (25,(27)(28)(29)(30).…”

Section: Discussionmentioning

confidence: 99%

Insulin and Angiotensin II Induce the Translocation of Scavenger Receptor Class B, Type I from Intracellular Sites to the Plasma Membrane of Adipocytes

Tondu

Robichon

Yvan‐Charvet

et al. 2005

Journal of Biological Chemistry

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Scavenger receptor class B, type I (SR-BI) mediates the selective uptake of lipids from high density lipoproteins and is expressed in several types of tissues. However, to date little is known about its role in adipocytes. In this study, we investigated the cellular distribution of SR-BI in 3T3-L1 adipocytes and its regulation by hormones known to increase lipid storage such as angiotensin II (Ang II) and insulin. SR-BI was mainly distributed in the cytoplasm as determined by laser-scanning confocal analysis of the immunofluorescence labeling of SR-BI or the study of an enhanced green fluorescent protein-tagged SR-BI fusion protein. Exposure of cells to either insulin or Ang II (1-2 h) induced the mobilization of SR-BI from intracellular pools to the plasma membrane. This was further confirmed by Western blotting on purified plasma membrane and by fluorescence-activated cell sorter analysis of the SR-BI receptor. Similar results were also observed in primary adipocytes. We also demonstrated that, in the presence of either insulin or Ang II, SR-BI translocation to the cell membrane is functional, because insulin and Ang II induced a significant increase in the high density lipoprotein-delivered 22-(N-7-nitrobenz-2-oxa-1,3-diazo-4-yl)-amino-23,24-bisnor-5-cholen-3-ol uptake and in total cholesterol content. These data demonstrate that SR-BI can be acutely mobilized from intracellular stores to the cell surface by insulin or Ang II, two hormones that exert lipogenic effects in adipocytes. This suggests that SR-BI might participate in the storage of lipids in the adipose tissue. Scavenger receptor class B, type I (SR-BI)2 is a membrane protein that can bind various classes of modified and unmodified lipoproteins. High density lipoproteins (HDLs), to which SR-BI binds with high affinity, are now considered as its physiological ligands (1, 2). As a consequence of HDL binding, it has been shown that SR-BI mediates the selective uptake of cholesteryl esters, a process that clearly differs from the low density lipoprotein receptor endocytic pathway (3, 4). SR-BI is particularly abundant in several tissues, including the liver and steroidogenic tissue (4). Several studies have reported a determinant role for hepatic SR-BI in the control of HDL cholesterol. Thus, mice lacking a functional SR-BI gene have increased levels of plasma cholesterol, whereas overexpression of SR-BI in mouse liver by adenovirus injection lowers HDL levels and increases biliary cholesterol (5-8). Modulation of SR-BI expression in vivo has also revealed that in steroidogenic tissues this receptor plays a major role in delivering cholesterol to be used for the synthesis of steroid hormones (4). These studies have left unresolved the role of this receptor in adipose tissue known to express SR-BI (9). SR-BI is also expressed in adipocyte cell lines and is strongly induced during the course of adipose differentiation, suggesting a role for SR-BI in the fully differentiated adipocyte (9).To get some insight into the function of SR-BI in adipocytes, we st...

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Angiotensin II Promotes Selective Uptake of High Density Lipoprotein Cholesterol Esters in Bovine Adrenal Glomerulosa and Human Adrenocortical Carcinoma Cells Through Induction of Scavenger Receptor Class B Type I

Cited by 24 publications

References 48 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

Prediabetic and diabetic in vivo modification of circulating low-density lipoprotein attenuates its stimulatory effect on adrenal aldosterone and cortisol secretion

Insulin and Angiotensin II Induce the Translocation of Scavenger Receptor Class B, Type I from Intracellular Sites to the Plasma Membrane of Adipocytes

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