Transfer of cholesterol between high density lipoproteins and cultured rat Sertoli cells

1996 ◽  
Vol 74 (5) ◽  
pp. 681-686 ◽  
Author(s):  
Mohamed Fofana ◽  
Jean-Claude Maboundou ◽  
Jean Bocquet ◽  
Dominique Le Goff
Keyword(s):  
Sertoli Cells ◽  
Hdl Cholesterol ◽  
High Density ◽  
High Density Lipoproteins ◽  
Phospholipid Vesicle ◽  
Steroid Production ◽  
Blood Capillaries ◽  
Apo E ◽  
Net Uptake

In the testes, the Sertoli cells are separated from the blood capillaries by the basement membrane, thereby excluding the passage of low density lipoproteins (LDLs) but allowing the passage of high density lipoproteins (HDLs). The present study examines first the capacity of Sertoli cells to uptake cholesterol from HDL and secondly the role of apolipoproteins (apo) A-I and E in cholesterol flux between HDL and cultured rat Sertoli cells. In the presence of HDL in cultured medium, rat Sertoli cells accumulated few amounts of esterified cholesterol. Incubation of [14C]cholesterol–labelled Sertoli cells with [3H]cholesterol–labelled HDL showed that the amount of cholesterol influx slightly exceeded its efflux, thus resulting in a net uptake of cholesterol from HDL to rat Sertoli cells. The amount of HDL–cholesterol converted to steroids by Sertoli cells was about 32% of influx. Uptake of cholesterol by Sertoli cells was three times higher with phospholipid – apo A-I vesicles and seven times higher with phospholipid – apo E vesicles than that with phospholipid vesicles without apolipoprotein. Phospholipid – apo A-I vesicles promoted cholesterol efflux at the same rate as native HDL and twice as efficiently as phospholipid – apo E vesicles. Thus, this study shows that rat Sertoli cells have the capacity to take up HDL–cholesterol for membrane renewal and steroid production mainly by apo E dependent pathways.Key words: apolipoproteins, cholesterol flux, phospholipid vesicle, steroid, testis.

Effect of lipoproteins on cholesterol synthesis in rat Sertoli cells

1995 ◽  
Vol 73 (1-2) ◽  
pp. 67-72 ◽  
Author(s):  
Jean-Claude Maboundou ◽  
Mohamed Fofana ◽  
Jacqueline Fresnel ◽  
Jean Bocquet ◽  
Dominique Le Goff
Keyword(s):  
Sertoli Cells ◽  
Free Cholesterol ◽  
Low Density Lipoproteins ◽  
High Density ◽  
High Density Lipoproteins ◽  
Low Density ◽  
Coated Pits ◽  
Apo B ◽  
Blood Capillaries ◽  
Apo E

Lipoprotein metabolism has been investigated in cultured rat Sertoli cells. Cells incubated with low-density lipoproteins (LDLs) or high-density lipoproteins (HDLs) showed a concentration-dependent decrease of sterol synthesis, indicating a net cholesterol delivery to the Sertoli cells. At 50 μg/mL, lipoproteins inhibited the incorporation of [14C]acetate into free cholesterol by 83% for the LDL and 47% for the HDL. Electron microscopic examinations of the Sertoli cells provide evidence of the internalization of gold-labelled HDL into coated pits and coated vesicles. Competitive studies between human LDL and rat HDL indicate that Sertoli cells take up cholesterol from LDL and HDL containing apolipoprotein (apo) E by common pathways. These results suggest that Sertoli cells possess apo B and E receptors for the uptake and degradation of LDL and HDL, although the basement membrane excludes the passage of LDL from blood capillaries to the Sertoli cells. At 50 μg/mL, apo-E-depleted HDL inhibited the incorporation of [14C]acetate into free cholesterol by 34%. Thus, this study shows that Sertoli cells are capable of taking up apo-E-depleted HDL cholesterol for cell metabolism.Key words: high-density lipoproteins, low-density lipoproteins, rat Sertoli cell.

scholarly journals Importance of Apolipoprotein A-I and A-II Composition in HDL and Its Potential for Studying COVID-19 and SARS-CoV-2

Medicines ◽  
2021 ◽  
Vol 8 (7) ◽  
pp. 38
Author(s):  
Kyung-Hyun Cho
Keyword(s):  
Antiviral Activity ◽  
High Density ◽  
High Density Lipoproteins ◽  
Potent Antiviral Activity ◽  
Apolipoprotein A ◽  
Putative Role

The composition and properties of apolipoprotein (apo) A-I and apoA-II in high-density lipoproteins (HDL) might be critical to SARS-CoV-2 infection via SR-BI and antiviral activity against COVID-19. HDL containing native apoA-I showed potent antiviral activity, while HDL containing glycated apoA-I or other apolipoproteins did not. However, there has been no report to elucidate the putative role of apoA-II in the antiviral activity of HDL.

scholarly journals High-Density Lipoproteins and the Kidney

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 764
Author(s):  
Arianna Strazzella ◽  
Alice Ossoli ◽  
Laura Calabresi
Keyword(s):  
Kidney Disease ◽  
Renal Disease ◽  
Cholesterol Acyltransferase ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
High Density ◽  
High Density Lipoproteins ◽  
Lcat Deficiency ◽  
Progression Of Renal Disease ◽  
The Impact

Dyslipidemia is a typical trait of patients with chronic kidney disease (CKD) and it is typically characterized by reduced high-density lipoprotein (HDL)-cholesterol(c) levels. The low HDL-c concentration is the only lipid alteration associated with the progression of renal disease in mild-to-moderate CKD patients. Plasma HDL levels are not only reduced but also characterized by alterations in composition and structure, which are responsible for the loss of atheroprotective functions, like the ability to promote cholesterol efflux from peripheral cells and antioxidant and anti-inflammatory proprieties. The interconnection between HDL and renal function is confirmed by the fact that genetic HDL defects can lead to kidney disease; in fact, mutations in apoA-I, apoE, apoL, and lecithin–cholesterol acyltransferase (LCAT) are associated with the development of renal damage. Genetic LCAT deficiency is the most emblematic case and represents a unique tool to evaluate the impact of alterations in the HDL system on the progression of renal disease. Lipid abnormalities detected in LCAT-deficient carriers mirror the ones observed in CKD patients, which indeed present an acquired LCAT deficiency. In this context, circulating LCAT levels predict CKD progression in individuals at early stages of renal dysfunction and in the general population. This review summarizes the main alterations of HDL in CKD, focusing on the latest update of acquired and genetic LCAT defects associated with the progression of renal disease.

scholarly journals HDL-Mediated Lipid Influx to Endothelial Cells Contributes to Regulating Intercellular Adhesion Molecule (ICAM)-1 Expression and eNOS Phosphorylation

2018 ◽  
Vol 19 (11) ◽  
pp. 3394 ◽  
Author(s):  
Mónica Muñoz-Vega ◽  
Felipe Massó ◽  
Araceli Páez ◽  
Gilberto Vargas-Alarcón ◽  
Ramón Coral-Vázquez ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Hdl Cholesterol ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
High Density Lipoproteins ◽  
Type I ◽  
Intercellular Adhesion Molecule 1 ◽  
Apo Ai

Reverse cholesterol transport (RCT) is considered as the most important antiatherogenic role of high-density lipoproteins (HDL), but interventions based on RCT have failed to reduce the risk of coronary heart disease. In contrast to RCT, important evidence suggests that HDL deliver lipids to peripheral cells. Therefore, in this paper, we investigated whether HDL could improve endothelial function by delivering lipids to the cells. Internalization kinetics using cholesterol and apolipoprotein (apo) AI fluorescent double-labeled reconstituted HDL (rHDL), and human dermal microvascular endothelial cells-1 (HMEC-1) showed a fast cholesterol influx (10 min) and a slower HDL protein internalization as determined by confocal microscopy and flow cytometry. Sphingomyelin kinetics overlapped that of apo AI, indicating that only cholesterol became dissociated from rHDL during internalization. rHDL apo AI internalization was scavenger receptor class B type I (SR-BI)-dependent, whereas HDL cholesterol influx was independent of SR-BI and was not completely inhibited by the presence of low-density lipoproteins (LDL). HDL sphingomyelin was fundamental for intercellular adhesion molecule-1 (ICAM-1) downregulation in HMEC-1. However, vascular cell adhesion protein-1 (VCAM-1) was not inhibited by rHDL, suggesting that components such as apolipoproteins other than apo AI participate in HDL’s regulation of this adhesion molecule. rHDL also induced endothelial nitric oxide synthase eNOS S1177 phosphorylation in HMEC-1 but only when the particle contained sphingomyelin. In conclusion, the internalization of HDL implies the dissociation of lipoprotein components and a SR-BI-independent fast delivery of cholesterol to endothelial cells. HDL internalization had functional implications that were mainly dependent on sphingomyelin. These results suggest a new role of HDL as lipid vectors to the cells, which could be congruent with the antiatherogenic properties of these lipoproteins.

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