Differences in the uptake of modified low density lipoproteins by tissue cultured endothelial cells

1985 ◽  
Vol 79 (1) ◽  
pp. 317-325
Author(s):  
J. Gaffney ◽  
D. West ◽  
F. Arnold ◽  
A. Sattar ◽  
S. Kumar
Keyword(s):  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Brain Capillary ◽  
Modified Low Density Lipoproteins ◽  
Lipoprotein Uptake ◽  
Ldl Uptake ◽  
Quantitative Examination

Acetylated low density lipoprotein (Ac-LDL) is taken up by bovine aortic and adrenal capillary cells but not by brain capillary cells. This indicates that the uptake of Ac-LDL is not a feature of all types of endothelial cell. A quantitative examination of lipoprotein uptake by flow cytometry showed cells in G2M took up 45% more Ac-LDL than those in G1S. Compared with confluent cultures, sub-confluent bovine aortic cells took up three times as much LDL but Ac-LDL uptake was increased by only 34%. This indicates that the Ac-LDL receptor is not down-regulated to the same extent as that for LDL.

scholarly journals Interaction of 4-hydroxynonenal-modified low-density lipoproteins with the fibroblast apolipoprotein B/E receptor

1986 ◽  
Vol 234 (1) ◽  
pp. 245-248 ◽  
Author(s):  
W Jessup ◽  
G Jurgens ◽  
J Lang ◽  
H Esterbauer ◽  
R T Dean
Keyword(s):  
Apolipoprotein B ◽  
Negative Charge ◽  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Low Density ◽  
Lipid Peroxidation Product ◽  
Modified Low Density Lipoproteins ◽  
Peroxidation Product

The incorporation of the lipid peroxidation product 4-hydroxynonenal into low-density lipoprotein (LDL) increases the negative charge of the particle, and decreases its affinity for the fibroblast LDL receptor. It is suggested that this modification may occur in vivo, and might promote atherogenesis.

scholarly journals LRP6 Protein Regulates Low Density Lipoprotein (LDL) Receptor-mediated LDL Uptake

2011 ◽  
Vol 287 (2) ◽  
pp. 1335-1344 ◽  
Author(s):  
Zhi-jia Ye ◽  
Gwang-Woong Go ◽  
Rajvir Singh ◽  
Wenzhong Liu ◽  
Ali Reza Keramati ◽  
...  
Keyword(s):  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Low Density ◽  
Ldl Uptake

scholarly journals Evidence for sterol-independent regulation of low-density lipoprotein receptor activity in Hep-G2 cells

1991 ◽  
Vol 279 (1) ◽  
pp. 175-187 ◽  
Author(s):  
J L Ellsworth ◽  
C Chandrasekaran ◽  
A D Cooper
Keyword(s):  
Low Density Lipoprotein ◽  
Calf Serum ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Low Density ◽  
Cholesteryl Esters ◽  
Hep G2 ◽  
Hep G2 Cells ◽  
Ldl Uptake ◽  
Stimulation Of

The relationship between the serum factor(s)-mediated induction of low-density lipoprotein (LDL) receptor activity and changes in cellular cholesterol metabolism was examined in the human hepatoma cell line Hep-G2. Relative to incubation with serum-free media [Eagle's minimal essential medium (MEM) control], short-term (less than 8 h) incubation with medium containing 15% of either calf serum (MEM + serum) or the d greater than 1.25 fraction of calf serum (MEM + d greater than 1.25) produced a time- and concentration-dependent increase in the uptake of 125I-LDL. Immunoblotting with anti-(LDL receptor) antibodies demonstrated that this was correlated with a 2-fold increase in the amount of the mature 136,000 Da LDL receptor protein in detergent-solubilized Hep-G2 cell membranes. Incubation with MEM + serum, but not MEM + d greater than 1.25, increased the efflux of radiolabelled cholesterol from Hep-G2 cells. However, the induction of 125I-LDL uptake by MEM + d greater than 1.25 (2.3-fold) and MEM + serum (2.2-fold) was virtually identical. Addition of the d less than 1.063 lipoproteins of calf serum to MEM + d greater than 1.25 at their original or three times their serum concentration decreased the induction of 125I-LDL uptake by MEM + d greater than 1.25 by only 20-30%. Together, these results suggest that the stimulation of 125I-LDL uptake was not due to the presence of high-density lipoprotein, the absence of LDL or the stimulation of cholesterol efflux. MEM + serum stimulated 125I-LDL uptake in cells cholesterol-loaded by incubation with rat very-low-density lipoprotein with beta electrophoretic mobility (beta-VLDL). Compared to incubation with the MEM control, either MEM + serum or MEM + d greater than 1.25 produced time-dependent increases in the activity of 3-hydroxy-3-methylglutaryl-CoA reductase which also occurred in cholesterol-loaded cells. However, cholesterol biosynthesis, whether measured from 3H2O, [14C]acetate or [3H]mevalonic acid, was not increased. Incubation with MEM + serum or MEM + d greater than 1.25 did not affect [3H]oleate incorporation into cellular cholesteryl esters, hydrolysis of intracellular [3H]cholesteryl esters or the cellular mass of unesterified or esterified cholesterol. Incubation with MEM + serum or MEM + d greater than 1.25 produced a transient increase in the level of LDL receptor mRNA, reaching a maximum of 5-10-fold by 2 h and decreasing to near baseline levels by 4 h. Actinomycin D blocked the serum-factor-mediated induction of LDL receptor mRNA.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Profile of Surrounding MicroRNAs in Low Density Lipoprotein Uptake

2017 ◽  
Author(s):  
Maria Elisabete Silva Santos ◽  
Ricardo Sousa De Oliveira Paraense ◽  
Eric Artur Cortinhas-Alves ◽  
Danilo Leôncio Aguiar Pereira
Keyword(s):  
Cardiovascular Disease ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Ldl Receptors ◽  
Lipid Metabolism Disorders ◽  
Lipoprotein Uptake ◽  
Ldl Uptake ◽  
Pcsk9 Inhibition ◽  
Potential Biomarkers

The atherosclerosis, a chronic and inflammatory disease that occurs when there are high levels of low-density lipoprotein (LDL) on plasma. This important risk factor for development of cardiovascular disease (CVD) is the main cause of death worldwide. MicroRNAs have recently emerged as potential biomarkers and therapeutic target for lipid metabolism disorders. In this review, we will provide profile of surrounding miRNAs that have demonstrated being regulators of PCSK9, LDLR and APOB100 genes. Recent work has identified the mir-148, mir-128, mir-27a/b, mir-185, mir-301, mir-130 as important regulators of this pathway because they decrease supply of LDL receptors through interaction with PCSK9. Inhibition of LDLR expression cause elevation of plasma LDL levels which induces atherosclerosis. While mir-30c, mir-122, mir-34 decrease MTTP, which promotes degradation of APOB100 preventing assembly and secretion of VLDL. We conclude that, when overexpressed, mir-148a, mir128 and mir-27a/b, mir-122 and mir-34 are related to decrease in LDLR, facilitating occurrence of atherosclerosis. While mir-30 has been linked to decreased atherosclerosis. Detection of miRNAs profile could be used in the future as a biomarker for disturbs linked to c-LDL uptake and in future anti-miRNAs therapies may be used in the treatment of atherosclerosis.

scholarly journals Profile of circulating MicroRNAs in low density lipoprotein uptake: literature review

2021 ◽  
Vol 13 (1) ◽  
pp. e4546
Author(s):  
Maria Elisabete Silva Santos ◽  
Ricardo Sousa de Oliveira Paraense ◽  
Ricardo Roberto de Souza Fonseca ◽  
Danilo Leôncio Aguiar Pereira ◽  
Carlos Eduardo Silva Cordeiro ◽  
...  
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Circulating Mirnas ◽  
Circulating Micrornas ◽  
Ldl Receptors ◽  
Lipid Metabolism Disorders ◽  
Lipoprotein Uptake ◽  
Ldl Uptake ◽  
Potential Biomarkers

Objective: Delineate a profile of circulating miRNA that interfere with the uptake of c-LDL through the regulation of LDL, APOB-100 and PCSK9 genes that can be used as biomarkers for prognosis and treatment of atherosclerosis. Bibliography review: The atherosclerosis, a chronic and inflammatory disease that occurs when there are high levels of LDL on plasma. This important risk factor for development of cardiovascular disease is the main cause of death worldwide. The miRNAs have recently emerged as potential biomarkers and therapeutic target for lipid metabolism disorders. In this review, we will provide profile of circulating miRNAs that have demonstrated being regulators of PCSK9, LDL and APOB100 genes. Recent work has identified the miR-148, miR-128, miR-27a/b, miR-185, miR-301, miR-130 as important regulators of this pathway because they decrease supply of LDL receptors through interaction with PCSK9. Final considerations: We conclude that, when overexpressed, miR-148a, mir128 and miR-27a/b, miR-122 and miR-34 are related to decrease in LDL, facilitating occurrence of atherosclerosis. Detection of miRNAs profile could be used in the future as a biomarker for disturbs linked to c-LDL uptake and in future anti-miRNAs therapies may be used in the treatment of atherosclerosis.

scholarly journals Trichomonas vaginalis is dependent on uptake and degradation of human low density lipoproteins.

1984 ◽  
Vol 160 (5) ◽  
pp. 1261-1272 ◽  
Author(s):  
K M Peterson ◽  
J F Alderete
Keyword(s):  
Trichomonas Vaginalis ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Surface Protein ◽  
Defined Medium ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Uptake Mechanism ◽  
Lipoprotein Subfractions ◽  
Lipoprotein Uptake

Human plasma low density lipoprotein uptake by the urogenital pathogen, Trichomonas vaginalis, was examined. Rapid binding and internalization of 125I-labeled low density lipoproteins by live T. vaginalis was observed at 37 degrees C. Data showing parasite degradation of the internalized apoproteins and lipid accumulation following low density lipoprotein uptake was obtained. Acquisition of low density lipoproteins was by a trichomonad surface protein that possessed a molecular weight of greater than 250,000. The receptor is specific for apolipoprotein CIII, a component of high, low, and very low density lipoprotein subfractions. Low density lipoproteins in a semi-defined medium of trypticase, nucleic acid precursors, vitamins, and maltose promoted T. vaginalis growth and multiplication at rates and levels equal to the yeast extract-trypticase-serum complex medium routinely used for culture of trichomonads. HeLa cell membranes as a source of lipids were unable to sustain T. vaginalis organisms. These data demonstrate host lipoprotein internalization by T. vaginalis via a specific uptake mechanism.

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