Association of low-density lipoprotein with particulate connective tissue matrix components enhances cholesterol accumulation in cultured subendothelial cells of human aorta
Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, ISSN: 0167-4889, Vol: 928, Issue: 3, Page: 251-258
1987
- 28Citations
- 7Captures
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Metrics Details
- Citations28
- Citation Indexes28
- CrossRef28
- 21
- Captures7
- Readers7
Article Description
Low-density lipoproteins (LDL) were incubated with elastin particles, collagenase-resistant debris isolated from human aorta, and latex beads of 1.13 μm in diameter. As a result of incubation, insoluble LDL-associates were formed. These associates, as well as LDL-heparin-fibronectin-gelatin complexes described by other workers, were added to a 7-day primary culture of enzyme-isolated cells of human aortic subendothelial intima. The culture contained a mixed cell population made up mostly of typical and modified smooth muscle cells. 24 h later, total cholesterol, phospholipid, triacylglycerol, free cholesterol and cholesteryl ester levels were measured. Addition of insoluble LDL-complexes as well as LDL-associates to culture brought about a substantial accumulation of intracellular lipids; primarily, cholesteryl esters. The total cholesterol level in cultured cells was raised 3- to 8-fold. Addition of free LDL or LDL-free particles had no effect on the content of intracellular lipids. The results obtained allow the assumption that the occurrence of the LDL-mediated accumulation of intracellular lipids is due mainly to the LDL penetration inside the cell via ‘nonspecific’ phagocytosis and not through a regulated receptor-dependent pathway.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/0167488987901832; http://dx.doi.org/10.1016/0167-4889(87)90183-2; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0023187167&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/3032280; https://linkinghub.elsevier.com/retrieve/pii/0167488987901832; http://dx.doi.org/10.1016/0167-4889%2887%2990183-2; https://dx.doi.org/10.1016/0167-4889%2887%2990183-2
Elsevier BV
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