Conjugates of colloidal gold with native and acetylated low density lipoproteins for ultrastructural investigations on receptor-mediated endocytosis by cultured human monocyte-derived macrophages

1985 ◽  
Vol 83 (1) ◽  
pp. 29-35 ◽  
Author(s):  
A. M. Mommaas-Kienhuis ◽  
J. G. Van der Schroeff ◽  
M. C. Wijsman ◽  
W. Th. Daems ◽  
B. J. Vermeer
Keyword(s):  
Colloidal Gold ◽  
Human Monocyte ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Receptor Mediated Endocytosis

scholarly journals The metabolism of native and malondialdehyde-altered low density lipoproteins by human monocyte-macrophages

1981 ◽  
Vol 22 (1) ◽  
pp. 63-71
Author(s):  
I Shechter ◽  
A M Fogelman ◽  
M E Haberland ◽  
J Seager ◽  
M Hokom ◽  
...  
Keyword(s):  
Human Monocyte ◽  
Low Density Lipoproteins ◽  
Low Density

scholarly journals Degradation of lipoproteins by human monocyte-derived macrophages. Evidence for two distinct processes for the degradation of abnormal very-low-density lipoprotein from subjects with type III hyperlipidaemia

1984 ◽  
Vol 218 (1) ◽  
pp. 101-111 ◽  
Author(s):  
A K Soutar ◽  
B L Knight
Keyword(s):  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Human Monocyte ◽  
Normal Subjects ◽  
Peritoneal Macrophages ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Free Medium ◽  
Very Low Density Lipoproteins ◽  
Type Iii

Human blood monocyte-derived macrophages that had been cultured in medium containing human serum for 7 days degraded the abnormal very-low-density lipoproteins (VLDL) from the plasma of subjects with type III hyperlipoproteinaemia by two distinct saturable processes. One process was stimulated when cells from normal subjects were preincubated with lipoprotein-free medium, was inhibited by excess unlabelled low-density lipoproteins (LDL) and was absent from cells from subjects with homozygous familial hypercholesterolaemia; on these criteria it was identified as an LDL-receptor-dependent process. Degradation by the second process was of equal magnitude in both cell types and was unaffected by excess unlabelled LDL or acetylated LDL. The activity of this process was reduced when the cells were preincubated in lipoprotein-free medium. The abnormal VLDL from the plasma of cholesterol-fed rabbits were also degraded by this process, which was similar to that in mouse peritoneal macrophages mediated by the receptor for VLDL of beta-electrophoretic mobility [Goldstein, Ho, Brown, Innerarity & Mahley (1980) J. Biol. Chem. 255, 1839-1848].

scholarly journals Effect of Exposure of Human Monocyte-Derived Macrophages to High, versus Normal, Glucose on Subsequent Lipid Accumulation from Glycated and Acetylated Low-Density Lipoproteins

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Fatemeh Moheimani ◽  
Joanne T. M. Tan ◽  
Bronwyn E. Brown ◽  
Alison K. Heather ◽  
David M. van Reyk ◽  
...  
Keyword(s):  
High Glucose ◽  
Lipid Accumulation ◽  
Scavenger Receptor ◽  
Ldl Receptor ◽  
Human Monocyte ◽  
Low Density Lipoproteins ◽  
Receptor Expression ◽  
Low Density ◽  
Cholesteryl Esters ◽  
Protein Levels

During atherosclerosis monocyte-derived macrophages accumulate cholesteryl esters from low-density lipoproteins (LDLs) via lectin-like oxidised LDL receptor-1 (LOX-1) and class AI and AII (SR-AI, SR-AII) and class B (SR-BI, CD36) scavenger receptors. Here we examined the hypothesis that hyperglycaemia may modulate receptor expression and hence lipid accumulation in macrophages. Human monocytes were matured into macrophages in 30 versus 5 mM glucose and receptor expression and lipid accumulation quantified. High glucose elevated LOX1 mRNA, but decreased SR-AI, SR-BI, LDLR, and CD36 mRNA. SR-BI and CD36 protein levels were decreased. Normo- and hyperglycaemic cells accumulated cholesteryl esters from modified LDL to a greater extent than control LDL, but total and individual cholesteryl ester accumulation was not affected by glucose levels. It is concluded that, whilst macrophage scavenger receptor mRNA and protein levels can be modulated by high glucose, these are not key factors in lipid accumulation by human macrophages under the conditions examined.

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