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Titolo:
Lp(a) and LDL induce apoptosis in human endothelial cells and in rabbit aorta: Role of oxidative stress
Autore:
Galle, J; Schneider, R; Heinloth, A; Wanner, C; Galle, PR; Conzelmann, E; Dimmeler, S; Heermeier, K;
Indirizzi:
Univ Hosp, Dept Med, Div Nephrol, D-97080 Wurzburg, Germany Univ Hosp Wurzburg Germany D-97080 iv Nephrol, D-97080 Wurzburg, Germany Univ Heidelberg Hosp, Dept Med, Div Gastroenterol, Heidelberg, Germany Univ Heidelberg Hosp Heidelberg Germany troenterol, Heidelberg, Germany Univ Frankfurt Klinikum, Dept Med, Div Cardiol, D-6000 Frankfurt, Germany Univ Frankfurt Klinikum Frankfurt Germany D-6000 6000 Frankfurt, Germany Univ Wurzburg, Dept Physiol Chem 2, Wurzburg, Germany Univ Wurzburg Wurzburg Germany , Dept Physiol Chem 2, Wurzburg, Germany
Titolo Testata:
KIDNEY INTERNATIONAL
fascicolo: 4, volume: 55, anno: 1999,
pagine: 1450 - 1461
SICI:
0085-2538(199904)55:4<1450:LALIAI>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
LOW-DENSITY-LIPOPROTEIN; SUPEROXIDE ANION PRODUCTION; ATHEROSCLEROTIC LESIONS; LIPID-PEROXIDATION; VITAMIN-E; IN-VIVO; DISEASE; DEATH; HYPERCHOLESTEROLEMIA; ACTIVATION;
Keywords:
lipoprotein; apoptosis; atherogenesis; superoxide radical; endothelium; lysophosphatidylcholine;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
55
Recensione:
Indirizzi per estratti:
Indirizzo: Galle, J Univ Hosp, Dept Med, Div Nephrol, Joseph Schneider Str 2, D-97080Wurzburg, Univ Hosp Joseph Schneider Str 2 Wurzburg Germany D-97080 zburg,
Citazione:
J. Galle et al., "Lp(a) and LDL induce apoptosis in human endothelial cells and in rabbit aorta: Role of oxidative stress", KIDNEY INT, 55(4), 1999, pp. 1450-1461

Abstract

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) [ip(a)] on O-2(-) formation and cell death in cultured human umbilical vein endothelial cells (HUVECs) and rabbit aorta (RA). Methods ann Results. O-2(-) 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 O-2(-) formation, increasing it in HUVECs by 356% at 5 mu g/ml and in RA by 294% at 100 mu g/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 aminimal effect on necrosis. nLp(a) elicited a small but significant effecton 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 O-2(-) formation was involved. The concentration of lysophosphatidylcholine, a lipoprotein oxidation product and stimulus for O-2(-) formation, was significantly enhanced by factor 5 in oxLDL and by factor 7 in oxLp(a) compared with native lipoproteins. Conclusion. Atherogenic lipoproteins stimulate O-2(-) formation and induction of apoptosis in HUVECs and RA, and may thereby influence the pathogenesis of atherosclerosis.

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Documento generato il 11/07/20 alle ore 17:37:33