Native and myeloperoxidase-oxidized low-density lipoproteins act in synergy to induce release of resolvin-D1 from endothelial cells

Damien Dufour, Alia Khalil, Vincent Nuyens, Alexandre Rousseau, Cédric Delporte, Caroline Noyon, Melissa Cortese, Florence Reyé, Valérie Pireaux, Jean Nève, Luc Vanhamme, Bernard Robaye, Christophe Lelubre, Jean Marc Desmet, Martine Raes, Karim Zouaoui Boudjeltia, Pierre Van Antwerpen

Résultats de recherche: Contribution à un journal/une revueArticle

Résumé

Background and aims: Oxidation of native low-density lipoproteins (LDLs-nat) plays an important role in the development of atherosclerosis. A major player in LDL-nat oxidation is myeloperoxidase (MPO), a heme enzyme present in azurophil granules of neutrophils and monocytes. MPO produces oxidized LDLs called Mox-LDLs, which cause a pro-inflammatory response in human microvascular endothelial cells (HMEC), monocyte/macrophage activation and formation of foam cells. Resolvin D1 (RvD1) is a compound derived from the metabolism of the polyunsaturated fatty acid DHA, which promotes resolution of inflammation at the ng/ml level. Methods: In the present study, we used liquid chromatography–mass spectrometry (LC-MS/MS) to investigate the synthesis of RvD1 and its precursors - 17(S)-hydroxy docosahexaenoic acid (17S-HDHA) and docosahexaenoic acid (DHA) - by HMEC, in the presence of several concentrations of Mox-LDLs, copper-oxidized-LDLs (Ox-LDLs), and native LDLs or in mouse plasma. The LC-MS/MS method has been validated and applied to cell supernatants and plasma to measure production of RvD1 and its precursors in several conditions. Results: Mox-LDLs played a significant role in the synthesis of RvD1 and 17S-HDHA from DHA compared to Ox-LDLs. Moreover, Mox-LDLs and LDLs-nat acted in synergy to produce RvD1. In addition, different correlations were found between RvD1 and M1 macrophages, age of mice or Cl-Tyr/Tyr ratio. Conclusions: These results suggest that although Mox-LDLs are known to be pro-inflammatory and deleterious in the context of atherosclerosis, they are also able to induce a pro-resolution effect by induction of RvD1 from HMEC. Finally, our data also suggest that HMEC can produce RvD1 on their own.

langue originaleAnglais
Pages (de - à)108-117
Nombre de pages10
journalAtherosclerosis
Volume272
Les DOIs
étatPublié - 1 mai 2018

Empreinte digitale

Peroxidase
Endothelial Cells
Docosahexaenoic Acids
Hydroxy Acids
Monocytes
Atherosclerosis
resolvin D1
oxidized low density lipoprotein
Foam Cells
Macrophage Activation
Plasma Cells
Unsaturated Fatty Acids
Heme
LDL Lipoproteins
Copper
Spectrum Analysis
Neutrophils
Macrophages
Inflammation
Enzymes

Citer ceci

Dufour, Damien ; Khalil, Alia ; Nuyens, Vincent ; Rousseau, Alexandre ; Delporte, Cédric ; Noyon, Caroline ; Cortese, Melissa ; Reyé, Florence ; Pireaux, Valérie ; Nève, Jean ; Vanhamme, Luc ; Robaye, Bernard ; Lelubre, Christophe ; Desmet, Jean Marc ; Raes, Martine ; Boudjeltia, Karim Zouaoui ; Van Antwerpen, Pierre. / Native and myeloperoxidase-oxidized low-density lipoproteins act in synergy to induce release of resolvin-D1 from endothelial cells. Dans: Atherosclerosis. 2018 ; Vol 272. p. 108-117.
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title = "Native and myeloperoxidase-oxidized low-density lipoproteins act in synergy to induce release of resolvin-D1 from endothelial cells",
abstract = "Background and aims: Oxidation of native low-density lipoproteins (LDLs-nat) plays an important role in the development of atherosclerosis. A major player in LDL-nat oxidation is myeloperoxidase (MPO), a heme enzyme present in azurophil granules of neutrophils and monocytes. MPO produces oxidized LDLs called Mox-LDLs, which cause a pro-inflammatory response in human microvascular endothelial cells (HMEC), monocyte/macrophage activation and formation of foam cells. Resolvin D1 (RvD1) is a compound derived from the metabolism of the polyunsaturated fatty acid DHA, which promotes resolution of inflammation at the ng/ml level. Methods: In the present study, we used liquid chromatography–mass spectrometry (LC-MS/MS) to investigate the synthesis of RvD1 and its precursors - 17(S)-hydroxy docosahexaenoic acid (17S-HDHA) and docosahexaenoic acid (DHA) - by HMEC, in the presence of several concentrations of Mox-LDLs, copper-oxidized-LDLs (Ox-LDLs), and native LDLs or in mouse plasma. The LC-MS/MS method has been validated and applied to cell supernatants and plasma to measure production of RvD1 and its precursors in several conditions. Results: Mox-LDLs played a significant role in the synthesis of RvD1 and 17S-HDHA from DHA compared to Ox-LDLs. Moreover, Mox-LDLs and LDLs-nat acted in synergy to produce RvD1. In addition, different correlations were found between RvD1 and M1 macrophages, age of mice or Cl-Tyr/Tyr ratio. Conclusions: These results suggest that although Mox-LDLs are known to be pro-inflammatory and deleterious in the context of atherosclerosis, they are also able to induce a pro-resolution effect by induction of RvD1 from HMEC. Finally, our data also suggest that HMEC can produce RvD1 on their own.",
keywords = "Atherosclerosis, Inflammation, Lipid mediators, Lipidomics, Low-density lipoproteins (LDLs), Myeloperoxidase, Omega-3 fatty acids, Tandem mass spectrometry",
author = "Damien Dufour and Alia Khalil and Vincent Nuyens and Alexandre Rousseau and C{\'e}dric Delporte and Caroline Noyon and Melissa Cortese and Florence Rey{\'e} and Val{\'e}rie Pireaux and Jean N{\`e}ve and Luc Vanhamme and Bernard Robaye and Christophe Lelubre and Desmet, {Jean Marc} and Martine Raes and Boudjeltia, {Karim Zouaoui} and {Van Antwerpen}, Pierre",
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pages = "108--117",
journal = "Atherosclerosis",
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Dufour, D, Khalil, A, Nuyens, V, Rousseau, A, Delporte, C, Noyon, C, Cortese, M, Reyé, F, Pireaux, V, Nève, J, Vanhamme, L, Robaye, B, Lelubre, C, Desmet, JM, Raes, M, Boudjeltia, KZ & Van Antwerpen, P 2018, 'Native and myeloperoxidase-oxidized low-density lipoproteins act in synergy to induce release of resolvin-D1 from endothelial cells', Atherosclerosis, VOL. 272, p. 108-117. https://doi.org/10.1016/j.atherosclerosis.2018.03.012

Native and myeloperoxidase-oxidized low-density lipoproteins act in synergy to induce release of resolvin-D1 from endothelial cells. / Dufour, Damien; Khalil, Alia; Nuyens, Vincent; Rousseau, Alexandre; Delporte, Cédric; Noyon, Caroline; Cortese, Melissa; Reyé, Florence; Pireaux, Valérie; Nève, Jean; Vanhamme, Luc; Robaye, Bernard; Lelubre, Christophe; Desmet, Jean Marc; Raes, Martine; Boudjeltia, Karim Zouaoui; Van Antwerpen, Pierre.

Dans: Atherosclerosis, Vol 272, 01.05.2018, p. 108-117.

Résultats de recherche: Contribution à un journal/une revueArticle

TY - JOUR

T1 - Native and myeloperoxidase-oxidized low-density lipoproteins act in synergy to induce release of resolvin-D1 from endothelial cells

AU - Dufour, Damien

AU - Khalil, Alia

AU - Nuyens, Vincent

AU - Rousseau, Alexandre

AU - Delporte, Cédric

AU - Noyon, Caroline

AU - Cortese, Melissa

AU - Reyé, Florence

AU - Pireaux, Valérie

AU - Nève, Jean

AU - Vanhamme, Luc

AU - Robaye, Bernard

AU - Lelubre, Christophe

AU - Desmet, Jean Marc

AU - Raes, Martine

AU - Boudjeltia, Karim Zouaoui

AU - Van Antwerpen, Pierre

PY - 2018/5/1

Y1 - 2018/5/1

N2 - Background and aims: Oxidation of native low-density lipoproteins (LDLs-nat) plays an important role in the development of atherosclerosis. A major player in LDL-nat oxidation is myeloperoxidase (MPO), a heme enzyme present in azurophil granules of neutrophils and monocytes. MPO produces oxidized LDLs called Mox-LDLs, which cause a pro-inflammatory response in human microvascular endothelial cells (HMEC), monocyte/macrophage activation and formation of foam cells. Resolvin D1 (RvD1) is a compound derived from the metabolism of the polyunsaturated fatty acid DHA, which promotes resolution of inflammation at the ng/ml level. Methods: In the present study, we used liquid chromatography–mass spectrometry (LC-MS/MS) to investigate the synthesis of RvD1 and its precursors - 17(S)-hydroxy docosahexaenoic acid (17S-HDHA) and docosahexaenoic acid (DHA) - by HMEC, in the presence of several concentrations of Mox-LDLs, copper-oxidized-LDLs (Ox-LDLs), and native LDLs or in mouse plasma. The LC-MS/MS method has been validated and applied to cell supernatants and plasma to measure production of RvD1 and its precursors in several conditions. Results: Mox-LDLs played a significant role in the synthesis of RvD1 and 17S-HDHA from DHA compared to Ox-LDLs. Moreover, Mox-LDLs and LDLs-nat acted in synergy to produce RvD1. In addition, different correlations were found between RvD1 and M1 macrophages, age of mice or Cl-Tyr/Tyr ratio. Conclusions: These results suggest that although Mox-LDLs are known to be pro-inflammatory and deleterious in the context of atherosclerosis, they are also able to induce a pro-resolution effect by induction of RvD1 from HMEC. Finally, our data also suggest that HMEC can produce RvD1 on their own.

AB - Background and aims: Oxidation of native low-density lipoproteins (LDLs-nat) plays an important role in the development of atherosclerosis. A major player in LDL-nat oxidation is myeloperoxidase (MPO), a heme enzyme present in azurophil granules of neutrophils and monocytes. MPO produces oxidized LDLs called Mox-LDLs, which cause a pro-inflammatory response in human microvascular endothelial cells (HMEC), monocyte/macrophage activation and formation of foam cells. Resolvin D1 (RvD1) is a compound derived from the metabolism of the polyunsaturated fatty acid DHA, which promotes resolution of inflammation at the ng/ml level. Methods: In the present study, we used liquid chromatography–mass spectrometry (LC-MS/MS) to investigate the synthesis of RvD1 and its precursors - 17(S)-hydroxy docosahexaenoic acid (17S-HDHA) and docosahexaenoic acid (DHA) - by HMEC, in the presence of several concentrations of Mox-LDLs, copper-oxidized-LDLs (Ox-LDLs), and native LDLs or in mouse plasma. The LC-MS/MS method has been validated and applied to cell supernatants and plasma to measure production of RvD1 and its precursors in several conditions. Results: Mox-LDLs played a significant role in the synthesis of RvD1 and 17S-HDHA from DHA compared to Ox-LDLs. Moreover, Mox-LDLs and LDLs-nat acted in synergy to produce RvD1. In addition, different correlations were found between RvD1 and M1 macrophages, age of mice or Cl-Tyr/Tyr ratio. Conclusions: These results suggest that although Mox-LDLs are known to be pro-inflammatory and deleterious in the context of atherosclerosis, they are also able to induce a pro-resolution effect by induction of RvD1 from HMEC. Finally, our data also suggest that HMEC can produce RvD1 on their own.

KW - Atherosclerosis

KW - Inflammation

KW - Lipid mediators

KW - Lipidomics

KW - Low-density lipoproteins (LDLs)

KW - Myeloperoxidase

KW - Omega-3 fatty acids

KW - Tandem mass spectrometry

UR - http://www.scopus.com/inward/record.url?scp=85044466810&partnerID=8YFLogxK

U2 - 10.1016/j.atherosclerosis.2018.03.012

DO - 10.1016/j.atherosclerosis.2018.03.012

M3 - Article

VL - 272

SP - 108

EP - 117

JO - Atherosclerosis

JF - Atherosclerosis

SN - 0021-9150

ER -