Document Detail

Oxidized low density lipoprotein stimulates aortic smooth muscle cell proliferation.
MedLine Citation:
PMID:  8724138     Owner:  NLM     Status:  MEDLINE    
We have investigated the effects of oxidized low density lipoproteins (Ox-LDL) on aortic smooth muscle cell (SMC) proliferation and the biosynthesis of glycosphingolipids. We found that Ox-LDL exerted a concentration, time, and temperature dependent alteration of cell proliferation and the biosynthesis of lactosylceramide. At low concentrations (5-10 micrograms/ml medium) Ox-LDL stimulated cell proliferation measured by an increase in the incorporation of [3H]-thymidine in cells and the synthesis of lactosylceramide, but not glucosylceramide synthesis. Oxidized LDL exerted a threefold increase in the incorporation of [3H]-galactose and [3H]-serine in lactosylceramide. The activity of lactosylceramide synthetase; UDP-galactose glucosylceramide beta 1 --> 4 galactosyltransferase (GalT-2), but not glucosylceramide synthetase (GlcT-1) was stimulated by Ox-LDL. On the other hand, LDL suppressed the activity of GalT-2 in these cells. When cells were preincubated with antibody against Ox-LDL or GalT-2 it compromised the Ox-LDL mediated stimulated in cell proliferation and GalT-2 activity. Similarly, D-PDMP an inhibitor of GalT-2 compromised the Ox-LDL mediated effects in cells. In contrast, L-PDMP further stimulated the Ox-LDL mediated cell proliferation and GalT-2 activity. However, preincubation of cells with preimmune rabbit serum IgG failed to abrogate Ox-LDL mediated stimulation in cell proliferation and GalT-2 activity. In sum, we found that Ox-LDL stimulated aortic smooth muscle cell proliferation in culture. This effect resulted from Ox-LDL mediated activation of GalT-2 that produced lactosylceramide. Lactosylceramide in turn, contributed to cell proliferation. Such correlations are supportive of the notion that GalT-2 action mediates the signal transduction of Ox-LDL contributing to cell proliferation.
S Chatterjee; N Ghosh
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Glycobiology     Volume:  6     ISSN:  0959-6658     ISO Abbreviation:  Glycobiology     Publication Date:  1996 Apr 
Date Detail:
Created Date:  1996-11-06     Completed Date:  1996-11-06     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  9104124     Medline TA:  Glycobiology     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  303-11     Citation Subset:  IM    
Lipid Research Atherosclerosis Unit, Johns Hopkins University, School of Medicine, Baltimore, MD 21287-3654, USA.
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MeSH Terms
Antibodies / pharmacology
Antigens, CD*
Aorta / cytology,  drug effects,  metabolism
Cell Division / drug effects
Enzyme Activation / drug effects
Enzyme Inhibitors / pharmacology
Galactose / metabolism
Galactosyltransferases / antagonists & inhibitors,  immunology,  metabolism
Glycoside Hydrolases / metabolism
Glycosyltransferases / metabolism
Lactosylceramides / biosynthesis
Lipoproteins, LDL / pharmacology*
Models, Biological
Morpholines / pharmacology
Muscle, Smooth, Vascular / cytology*,  drug effects*,  metabolism
Serine / metabolism
Signal Transduction
Thymidine / metabolism
Grant Support
Reg. No./Substance:
0/Antibodies; 0/Antigens, CD; 0/Enzyme Inhibitors; 0/Lactosylceramides; 0/Lipoproteins, LDL; 0/Morpholines; 0/oxidized low density lipoprotein; 26566-61-0/Galactose; 4682-48-8/CDw17 antigen; 50-89-5/Thymidine; 56-45-1/Serine; 73257-80-4/RV 538; EC 2.4.-/Glycosyltransferases; EC 2.4.1.-/Galactosyltransferases; EC 2.4.1.-/glucosylceramide beta-1-4-galactosyltransferase; EC 3.2.1.-/Glycoside Hydrolases

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