Document Detail

Lipoprotein and cholesterol metabolism in rabbit arterial endothelial cells in culture.
MedLine Citation:
PMID:  208629     Owner:  NLM     Status:  MEDLINE    
Like all other peripheral cells types thus far studied in culture, endothelial cells derived from the rabbit aorta bind, internalize and degrade low density lipoprotein (LDL) at a significant rate. At any given LDL concentration, the metabolism by rabbit endothelial cells was slower than that by fibroblasts or smooth muscle cells. Thus, longer incubations were required to achieve a net increment in cell cholesterol content or to suppress endogenous sterol synthesis; after 18-24 h incubation in the presence of LDL at 100 microgram LDL protein/ml inhibition was greater than 80% relative to the rate in cells incubated in the absence of lipoproteins. High density lipoproteins (HDL) were also taken up and degraded but did not inhibit sterol synthesis. Studies of LDL binding to the cell surface suggested the presence of at least two classes of binding sites; the high-affinity binding sites were fully saturated at very low LDL concentrations (about 5 microgram LDL protein/ml). However, the degree of inhibition of endogenous sterol synthesis increased progressively with increasing LDL concentrations from 5 to 100 microgram LDL/ml, suggesting that uptake from the low affinity sites in this cell line contributes to the suppression of endogenous sterol synthesis. The internalization and degradation of LDL also increased with concentrations as high as 700 microgram/ml. Thus, in vivo, where the cells are exposed to LDL concentrations far above that needed to saturate the high affinity sites, most of the LDL degradation would be attributable to LDL taken up from low affinity sites. As noted previously in swine arterial smooth muscle cells and in human skin fibroblasts, unlabeled HDL reduced the binding, internalization and degradation of labeled LDL. Cells incubated for 24 h in the presence of high concentrations of LDL alone showed a net increment in cell cholesterol content; the simultaneous presence of HDL in the medium significantly reduced this LDL-induced increment in cell cholesterol content. The possible relationship between LDL uptake and degradation by these cells in vitro is discussed in relationship to their transport function in vivo.
J P Reckless; D B Weinstein; D Steinberg
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Biochimica et biophysica acta     Volume:  529     ISSN:  0006-3002     ISO Abbreviation:  Biochim. Biophys. Acta     Publication Date:  1978 Jun 
Date Detail:
Created Date:  1978-09-30     Completed Date:  1978-09-30     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0217513     Medline TA:  Biochim Biophys Acta     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  475-87     Citation Subset:  IM    
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MeSH Terms
Acetates / metabolism
Aorta, Thoracic / cytology*,  metabolism
Cell Membrane / metabolism
Cholesterol / analogs & derivatives,  metabolism*,  pharmacology
Endothelium / metabolism*
Fatty Acids / biosynthesis
Lipoproteins / metabolism*
Lipoproteins, HDL / metabolism
Lipoproteins, LDL / metabolism
Protein Binding
Sterols / biosynthesis
Reg. No./Substance:
0/Acetates; 0/Fatty Acids; 0/Lipoproteins; 0/Lipoproteins, HDL; 0/Lipoproteins, LDL; 0/Sterols; 57-88-5/Cholesterol

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