Document Detail


Regulation of the selective uptake of high density lipoprotein-associated cholesteryl esters by human fibroblasts and Hep G2 hepatoma cells.
MedLine Citation:
PMID:  2846735     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We have previously shown that the liver and steroidogenic tissues of rats in vivo and a wider range of cells in vitro, including human cells, selectively take up high density lipoprotein (HDL) cholesteryl esters without parallel uptake of HDL particles. This process is regulated in tissues of rats and in cultured rat cells according to their cholesterol status. In the present study, we examined regulation of HDL selective uptake in cultured human fibroblasts and Hep G2 hepatoma cells. The cholesterol content of these cells was modified by a 20-hr incubation with either low density lipoprotein (LDL) or free cholesterol. Uptake of HDL components was examined in a subsequent 4-6-hr assay using intracellularly trapped tracers: 125I-labeled N-methyl-tyramine-cellobiose-apoA-I (125I-NMTC-apoA-I) to trace apoA-I, and [3H]cholesteryl oleyl ether to trace cholesteryl esters. In the case of fibroblasts, pretreatment with either LDL or free cholesterol resulted in decreased selective uptake (total [3H]cholesteryl ether uptake minus that due to particle uptake as measured by 125I-NMTC-apoA-I). In contrast, HDL particle uptake increased with either form of cholesterol loading. The amount of HDL that was reversibly cell-associated (bound) was increased by prior exposure to free cholesterol, but was decreased by prior exposure to LDL. In the case of Hep G2 cells, exposure to free cholesterol only slightly increased HDL particle uptake; selective uptake decreased after both forms of cholesterol loading, and reversibly bound HDL increased after exposure to free cholesterol, but either did not change or decreased after exposure to LDL. It was excluded that either LDL carried over into the HDL uptake assay or that products secreted by the cultured cells influenced these results. Thus, selective uptake by cells of both hepatic and extrahepatic origin was down-regulated by cholesterol loading, under which conditions HDL particle uptake increased. Total HDL binding was not directly correlated with either the rate of selective uptake or the rate of HDL particle uptake or the cholesterol status of the cells, suggesting more than one type of HDL binding site.
Authors:
F Rinninger; R C Pittman
Related Documents :
7712045 - Physiological role and clinical relevance of high-density lipoprotein subclasses.
11544085 - High density lipoprotein cholesteryl ester metabolism in the pony, an animal species wi...
12730295 - Alterations of plasma lipids in mice via adenoviral-mediated hepatic overexpression of ...
8246775 - Unusual high-density lipoprotein subclass distribution during late pregnancy.
15757005 - Constructions of therapist-client sex: a comparative analysis of retrospective victim r...
22703625 - Evaluation of endothelial dysfunction, lipid metabolism in women with polycystic ovary ...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of lipid research     Volume:  29     ISSN:  0022-2275     ISO Abbreviation:  J. Lipid Res.     Publication Date:  1988 Sep 
Date Detail:
Created Date:  1988-12-20     Completed Date:  1988-12-20     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0376606     Medline TA:  J Lipid Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1179-94     Citation Subset:  IM    
Affiliation:
Department of Medicine, University of California, San Diego, La Jolla 92093.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Carcinoma, Hepatocellular / metabolism*
Cholesterol Esters / metabolism*
Fibroblasts / metabolism
Homeostasis
Humans
Lipoproteins, HDL / metabolism*
Lipoproteins, LDL / metabolism
Liver Neoplasms
Rats
Grant Support
ID/Acronym/Agency:
HL-14197/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Cholesterol Esters; 0/Lipoproteins, HDL; 0/Lipoproteins, LDL

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Cell-surface binding sites for high density lipoproteins do not mediate efflux of cholesterol from h...
Next Document:  Apolipoprotein B synthesized by Hep G2 cells undergoes fatty acid acylation.