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6. Deletion of lysophosphatidylcholine acyltransferase 3 in myeloid cells worsens hepatic steatosis after a high-fat diet

Author

Bourgeois, Thibaut, Jalil, Antoine, Thomas, Charles, Magnani, Charlène, Le Guern, Naig, Gautier, Thomas, Pais de Barros, Jean-Paul, Bergas, Victoria, Choubley, Hélène, Mazzeo, Loïc, Menegaut, Louise, Josiane Lebrun, Lorène, Van Dongen, Kévin, Xolin, Marion, Jourdan, Tony, Buch, Chloé, Labbé, Jérome, Saas, Philippe, Lagrost, Laurent, Masson, David, Grober, Jacques, Lipides - Nutrition - Cancer [Dijon - U1231] (LNC), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement, Laboratoire d'Excellence : Lipoprotéines et Santé : prévention et Traitement des maladies Inflammatoires et du Cancer (LabEx LipSTIC), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut Gustave Roussy (IGR)-Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy)-Centre Hospitalier Régional Universitaire de Besançon (CHRU Besançon)-Université de Bourgogne (UB)-Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon)-Centre Régional de Lutte contre le cancer Georges-François Leclerc [Dijon] (UNICANCER/CRLCC-CGFL), UNICANCER-UNICANCER-Institut National de la Santé et de la Recherche Médicale (INSERM)-Fédération Francophone de la Cancérologie Digestive, FFCD-Université de Montpellier (UM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté])-Centre National de la Recherche Scientifique (CNRS)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Plateforme Lipidomique [Dijon] (LAP), Lipides - Nutrition - Cancer (U866) (LNC), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Ecole Nationale Supérieure de Biologie Appliquée à la Nutrition et à l'Alimentation de Dijon (ENSBANA)-IFR100 - Structure fédérative de recherche Santé-STIC-Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement, Interactions hôte-greffon-tumeur, ingénierie cellulaire et génique - UFC (UMR INSERM 1098) (RIGHT), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté]), Laboratoire de biochimie médicale (CHU de Dijon), Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), Université de Bourgogne (UB)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté])-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Laboratoire de biochimie médicale (CHU Dijon), and Dijon, Institut Agro

Subjects
obesity, AA, arachidonic acid, QD415-436, Biochemistry, LPCAT3, lysophosphatidylcholine acyltransferase 3, PC, phosphatidylcholine, insulin resistance, lipid metabolism, [SDV.IDA]Life Sciences [q-bio]/Food engineering, arachidonic acid, steatosis, LPLAT, lyso-PL-acyltransferase, phospholipid, lysophosphatidylcholine acyltransferase 3 (LPCAT3), 1-Acylglycerophosphocholine O-Acyltransferase, [SDV.IDA] Life Sciences [q-bio]/Food engineering, PS, phosphatidylserine, macrophages, pPE, plasmalogen, [SDV.AEN] Life Sciences [q-bio]/Food and Nutrition, inflammation, LPS, lipopolysaccharide, PL, phosphatidylinositol, lipids (amino acids, peptides, and proteins), LXR, liver X receptor, atherosclerosis, [SDV.AEN]Life Sciences [q-bio]/Food and Nutrition, Research Article
Abstract

International audience; Recent studies have highlighted an important role for lysophosphatidylcholine acyltransferase 3 (LPCAT3) in controlling the PUFA composition of cell membranes in the liver and intestine. In these organs, LPCAT3 critically supports cell-membrane-associated processes such as lipid absorption or lipoprotein secretion. However, the role of LPCAT3 in macrophages remains controversial. Here, we investigated LPCAT3's role in macrophages both in vitro and in vivo in mice with atherosclerosis and obesity. To accomplish this, we used the LysMCre strategy to develop a mouse model with conditional Lpcat3 deficiency in myeloid cells (Lpcat3KOMac). We observed that partial Lpcat3 deficiency (approximately 75% reduction) in macrophages alters the PUFA composition of all phospholipid (PL) subclasses, including phosphatidylinositols and phosphatidylserines. A reduced incorporation of C20 PUFAs (mainly arachidonic acid [AA]) into PLs was associated with a redistribution of these FAs toward other cellular lipids such as cholesteryl esters. Lpcat3 deficiency had no obvious impact on macrophage inflammatory response or endoplasmic reticulum (ER) stress; however, Lpcat3KOMac macrophages exhibited a reduction in cholesterol efflux in vitro. In vivo, myeloid Lpcat3 deficiency did not affect atherosclerosis development in LDL receptor deficient mouse (Ldlr-/-) mice. Lpcat3KOMac mice on a high-fat diet displayed a mild increase in hepatic steatosis associated with alterations in several liver metabolic pathways and in liver eicosanoid composition. We conclude that alterations in AA metabolism along with myeloid Lpcat3 deficiency may secondarily affect AA homeostasis in the whole liver, leading to metabolic disorders and triglyceride accumulation.

Published
2021

7. Inhibition of mitophagy drives macrophage activation and antibacterial defense during sepsis

Author

Patoli, Danish, primary, Mignotte, Franck, additional, Deckert, Valérie, additional, Dusuel, Alois, additional, Dumont, Adélie, additional, Rieu, Aurélie, additional, Jalil, Antoine, additional, Van Dongen, Kevin, additional, Bourgeois, Thibaut, additional, Gautier, Thomas, additional, Magnani, Charlène, additional, Le Guern, Naig, additional, Mandard, Stéphane, additional, Bastin, Jean, additional, Djouadi, Fatima, additional, Schaeffer, Christine, additional, Guillaumot, Nina, additional, Narce, Michel, additional, Nguyen, Maxime, additional, Guy, Julien, additional, Dargent, Auguste, additional, Quenot, Jean-Pierre, additional, Rialland, Mickaël, additional, Masson, David, additional, Auwerx, Johan, additional, Lagrost, Laurent, additional, and Thomas, Charles, additional

Published
2020
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8. Interplay between Liver X Receptor and Hypoxia Inducible Factor 1α Potentiates Interleukin-1β Production in Human Macrophages

Author

Ménégaut, Louise, primary, Thomas, Charles, additional, Jalil, Antoine, additional, Julla, Jean Baptiste, additional, Magnani, Charlène, additional, Ceroi, Adam, additional, Basmaciyan, Louise, additional, Dumont, Adélie, additional, Le Goff, Wilfried, additional, Mathew, Mano Joseph, additional, Rébé, Cédric, additional, Dérangère, Valentin, additional, Laubriet, Aline, additional, Crespy, Valentin, additional, Pais de Barros, Jean-Paul, additional, Steinmetz, Eric, additional, Venteclef, Nicolas, additional, Saas, Philippe, additional, Lagrost, Laurent, additional, and Masson, David, additional

Published
2020
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10. Deletion of lysophosphatidylcholine acyltransferase 3 in myeloid cells worsens hepatic steatosis after a high-fat diet.

Author

Bourgeois T, Jalil A, Thomas C, Magnani C, Le Guern N, Gautier T, Pais de Barros JP, Bergas V, Choubley H, Mazzeo L, Menegaut L, Josiane Lebrun L, Van Dongen K, Xolin M, Jourdan T, Buch C, Labbé J, Saas P, Lagrost L, Masson D, and Grober J

Abstract

Recent studies have highlighted an important role for lysophosphatidylcholine acyltransferase 3 (LPCAT3) in controlling the PUFA composition of cell membranes in the liver and intestine. In these organs, LPCAT3 critically supports cell-membrane-associated processes such as lipid absorption or lipoprotein secretion. However, the role of LPCAT3 in macrophages remains controversial. Here, we investigated LPCAT3's role in macrophages both in vitro and in vivo in mice with atherosclerosis and obesity. To accomplish this, we used the LysMCre strategy to develop a mouse model with conditional Lpcat3 deficiency in myeloid cells (Lpcat3KO Mac ). We observed that partial Lpcat3 deficiency (approximately 75% reduction) in macrophages alters the PUFA composition of all phospholipid (PL) subclasses, including phosphatidylinositols and phosphatidylserines. A reduced incorporation of C20 PUFAs (mainly arachidonic acid [AA]) into PLs was associated with a redistribution of these FAs toward other cellular lipids such as cholesteryl esters. Lpcat3 deficiency had no obvious impact on macrophage inflammatory response or endoplasmic reticulum (ER) stress; however, Lpcat3KO Mac macrophages exhibited a reduction in cholesterol efflux in vitro. In vivo, myeloid Lpcat3 deficiency did not affect atherosclerosis development in LDL receptor deficient mouse (Ldlr -/- ) mice. Lpcat3KO Mac mice on a high-fat diet displayed a mild increase in hepatic steatosis associated with alterations in several liver metabolic pathways and in liver eicosanoid composition. We conclude that alterations in AA metabolism along with myeloid Lpcat3 deficiency may secondarily affect AA homeostasis in the whole liver, leading to metabolic disorders and triglyceride accumulation., Competing Interests: Conflict of interest The authors declare that they have no conflicts of interest with the contents of this article., (Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.)

Published
2021
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