Document Detail


Lp(a) and LDL induce apoptosis in human endothelial cells and in rabbit aorta: role of oxidative stress.
MedLine Citation:
PMID:  10201010     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Atherogenic lipoproteins cause injury to the vascular wall in the early phase of atherogenesis. We assessed the effects of native (nLDL) and oxidized (oxLDL) low-density lipoprotein (LDL) and lipoprotein (a) [Lp(a)] on O2- formation and cell death in cultured human umbilical vein endothelial cells (HUVECs) and rabbit aorta (RA). METHODS AND RESULTS: O2- formation of HUVECs and RA segments was not influenced by nLDL, but was dose dependently increased by oxLDL and was moderately increased by nLp(a). oxLp(a) was the most potent stimulus for O2- formation, increasing it in HUVECs by 356% at 5 micrograms/ml and in RA by 294% at 100 micrograms/ml. Apoptosis was detected by DNA fragmentation and Annexin assay in HUVECs and by TUNEL staining in RA. Incubation of HUVECs and RA with oxLDL, but not nLDL, dose and time dependently induced apoptosis with only a minimal effect on necrosis. nLp(a) elicited a small but significant effect on apoptosis, whereas oxLp(a) induced apoptosis more potently than oxLDL in HUVECs and RA and caused necrotic cell death in HUVECs. Induction of apoptosis by oxLDL and oxLp(a) in RA was enhanced by the superoxide dismutase (SOD) inhibitor, diethyl-dithio-carbamate, and was blunted by SOD and catalase in HUVECs and RA, suggesting that O2- formation was involved. The concentration of lysophosphatidylcholine, a lipoprotein oxidation product and stimulus for O2- formation, was significantly enhanced by factor 5 in oxLDL and by factor 7 in oxLp(a) compared with native lipoproteins. CONCLUSION: Atherogenic lipoproteins stimulate O2- formation and induction of apoptosis in HUVECs and RA, and may thereby influence the pathogenesis of atherosclerosis.
Authors:
J Galle; R Schneider; A Heinloth; C Wanner; P R Galle; E Conzelmann; S Dimmeler; K Heermeier
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Kidney international     Volume:  55     ISSN:  0085-2538     ISO Abbreviation:  Kidney Int.     Publication Date:  1999 Apr 
Date Detail:
Created Date:  1999-07-14     Completed Date:  1999-07-14     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0323470     Medline TA:  Kidney Int     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1450-61     Citation Subset:  IM    
Affiliation:
Department of Medicine, University Hospital of Würzburg, Germany. j-c.galle@mail.uni-WUERZBURG.DE
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MeSH Terms
Descriptor/Qualifier:
Animals
Antioxidants / pharmacology
Aorta / cytology,  drug effects*
Apoptosis*
Catalase / pharmacology
Chemiluminescent Measurements
Endothelium, Vascular / cytology,  drug effects*
Female
Humans
Lipoprotein(a) / pharmacology*
Lipoproteins, LDL / pharmacology*
Lysophosphatidylcholines / biosynthesis,  pharmacology
Male
Oxidation-Reduction / drug effects
Oxidative Stress / physiology*
Rabbits
Superoxide Dismutase / pharmacology
Superoxides / metabolism
Chemical
Reg. No./Substance:
0/Antioxidants; 0/Lipoprotein(a); 0/Lipoproteins, LDL; 0/Lysophosphatidylcholines; 0/oxidized low density lipoprotein; 11062-77-4/Superoxides; EC 1.11.1.6/Catalase; EC 1.15.1.1/Superoxide Dismutase

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


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