Oxidized low-density-lipoprotein triggers programmed death of endothelial cells.
Incubation of bovine aortic as well as human umbilical vein endothelial cells with either oxidized or native low-density-lipoprotein in the presence of trace amounts of copper induced morphological changes of the cells and chromatin fragmentation characteristic for programmed cell death. Shrinkage of cells was evident after 6 to 8 hours of incubation and clearly preceded release of lactate dehydrogenase as a marker of cell permeability. Condensation of nuclear chromatin and internucleosomal cleavage was demonstrated by Hoechst staining and gel electrophoresis, respectively. Thus, by inducing active death of endothelial cells oxidized low-density-lipoprotein might negatively influence tissue homeostasis of the endothelium and thereby promote the development of atherosclerotic plaques.
Seelos
C
C
Institute of Tumorbiology-Cancer Research, University of Vienna, Austria.
Gmeiner
B
B
Kapiotis
S
S
Cerni
C
C
D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002417:Cattle; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008077:Lipoproteins, LDL / Q000494:pharmacology*
D008077:Lipoproteins, LDL; C099252:oxidized low density lipoprotein; D007770:L-Lactate Dehydrogenase