caa a22 4500 606220658 CHVBK 20210128101124.0 cr unu---uuuuu 210128e20151101xx s 000 0 eng 10.1007/s00380-014-0543-2 doi (NATIONALLICENCE)springer-10.1007/s00380-014-0543-2 Oxidation-induced loss of the ability of HDL to counteract the inhibitory effect of oxidized LDL on vasorelaxation [Elektronische Daten] [Laurence Perségol, Marie-Claude Brindisi, David Rageot, Jean-Paul Pais de Barros, Serge Monier, Bruno Vergès, Laurence Duvillard] Several current diseases are associated with an increase in the oxidation of HDL, which is likely to impair their functionality. Our aim was to identify whether oxidation could change the protective effect of HDL against the deleterious effect on vasoreactivity induced by oxidative stress. HDL from healthy subjects were oxidized in vitro by Cu2+, and the ability of oxidized HDL to counteract the inhibitory effect of oxidized LDL on acetylcholine-induced vasodilation was tested on isolated rabbit aorta rings. Oxidation of HDL was evidenced by the increase in the 7-oxysterols/cholesterol ratio (3.20±1.12 vs 0.02±0.01% in native HDL, p<0.05). Oxidized LDL inhibited endothelium-dependent vasodilation (E max=50.2±5.0 vs 92.5±1.7% for incubation in Kreb's buffer, p<0.05) and native HDL counteracted this inhibition (E max=72.4±4.8 vs 50.2±5.0% p<0.05). At the opposite, oxidized HDL had no effect on oxidized LDL-induced inhibition on endothelium-dependent vasorelaxation (E max=53.7±4.8 vs 50.2±5.0%, NS). HDL oxidation is associated with a decreased ability of HDL to remove 7-oxysterols from oxidized LDL. In conclusion, these results show that oxidation of HDL induces the loss of their protective effect against endothelial dysfunction, which could promote atherosclerosis in diseases associated with increased oxidative stress. Springer Japan, 2014 Oxidized HDL nationallicence Oxidized LDL nationallicence Vasorelaxation nationallicence Rabbit aorta rings nationallicence Perségol Laurence Faculté de Médecine, INSERM U866-Université de Bourgogne, 21000, Dijon, France aut Brindisi Marie-Claude Faculté de Médecine, INSERM U866-Université de Bourgogne, 21000, Dijon, France aut Rageot David Plateforme Lipidomique, Structure Fédérative de Recherche, 21000, Dijon, France aut Pais de Barros Jean-Paul Plateforme Lipidomique, Structure Fédérative de Recherche, 21000, Dijon, France aut Monier Serge Faculté de Médecine, INSERM U866-Université de Bourgogne, 21000, Dijon, France aut Vergès Bruno Faculté de Médecine, INSERM U866-Université de Bourgogne, 21000, Dijon, France aut Duvillard Laurence Faculté de Médecine, INSERM U866-Université de Bourgogne, 21000, Dijon, France aut Heart and Vessels Springer Japan 30/6(2015-11-01), 845-849 0910-8327 30:6<845 2015 30 380 https://doi.org/10.1007/s00380-014-0543-2 text/html Onlinezugriff via DOI BK010053 XK010053 XK010000 Metadata rights reserved Springer special CC-BY-NC licence nationallicence 1 brief-communication jats NATIONALLICENCE NATIONALLICENCE NL-springer NATIONALLICENCE 856 40 https://doi.org/10.1007/s00380-014-0543-2 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Perségol Laurence Faculté de Médecine, INSERM U866-Université de Bourgogne, 21000, Dijon, France aut NATIONALLICENCE 700 1- Brindisi Marie-Claude Faculté de Médecine, INSERM U866-Université de Bourgogne, 21000, Dijon, France aut NATIONALLICENCE 700 1- Rageot David Plateforme Lipidomique, Structure Fédérative de Recherche, 21000, Dijon, France aut NATIONALLICENCE 700 1- Pais de Barros Jean-Paul Plateforme Lipidomique, Structure Fédérative de Recherche, 21000, Dijon, France aut NATIONALLICENCE 700 1- Monier Serge Faculté de Médecine, INSERM U866-Université de Bourgogne, 21000, Dijon, France aut NATIONALLICENCE 700 1- Vergès Bruno Faculté de Médecine, INSERM U866-Université de Bourgogne, 21000, Dijon, France aut NATIONALLICENCE 700 1- Duvillard Laurence Faculté de Médecine, INSERM U866-Université de Bourgogne, 21000, Dijon, France aut NATIONALLICENCE 773 0- Heart and Vessels Springer Japan 30/6(2015-11-01), 845-849 0910-8327 30:6<845 2015 30 380