Nucleotide-binding oligomerization domain ...
Type de document :
Article dans une revue scientifique: Article original
PMID :
URL permanente :
Titre :
Nucleotide-binding oligomerization domain 1 (NOD1) modulates liver ischemia reperfusion through the expression adhesion molecules.
Auteur(s) :
Lassailly, Guillaume [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Bou Saleh, Mohamed [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Chavain, Natascha [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Ningarhari, Massih [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Gantier, EMILIE [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Carpentier, Rodolphe [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Artru, Florent [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Gnemmi, Viviane [Auteur]
Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer (JPArc) - U1172
Bertin, Benjamin [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Maboudou, Patrice [Auteur]
Betbeder, Didier [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Gheeraert, Celine [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Maggiotto, Francois [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Dharancy, Sebastien [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Mathurin, Philippe [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Louvet, Alexandre [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Dubuquoy, Laurent [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Lille Inflammation Research International Center - U 995 [LIRIC]
Bou Saleh, Mohamed [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Chavain, Natascha [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Ningarhari, Massih [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Gantier, EMILIE [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Carpentier, Rodolphe [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Artru, Florent [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Gnemmi, Viviane [Auteur]
Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer (JPArc) - U1172
Bertin, Benjamin [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Maboudou, Patrice [Auteur]
Betbeder, Didier [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Gheeraert, Celine [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Maggiotto, Francois [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Dharancy, Sebastien [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Mathurin, Philippe [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Louvet, Alexandre [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Dubuquoy, Laurent [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Titre de la revue :
Journal of hepatology
Nom court de la revue :
J. Hepatol.
Date de publication :
2019-01-24
ISSN :
1600-0641
Discipline(s) HAL :
Sciences du Vivant [q-bio]
Résumé en anglais : [en]
In liver transplantation, organ shortage leads to the use of marginal grafts that are more susceptible to ischemia-reperfusion (IR) injury. We identified nucleotide-binding oligomerization domain 1 (NOD1) as an important ...
Lire la suite >In liver transplantation, organ shortage leads to the use of marginal grafts that are more susceptible to ischemia-reperfusion (IR) injury. We identified nucleotide-binding oligomerization domain 1 (NOD1) as an important modulator of polymorphonuclear neutrophil (PMN)-induced liver injury, which occurs in IR. Herein, we aimed to elucidate the role of NOD1 in IR injury, particularly focusing on its effects on the endothelium and hepatocytes.Nod1 WT and KO mice were treated with NOD1 agonists and subjected to liver IR. Expression of adhesion molecules was analyzed in total liver, isolated hepatocytes and endothelial cells. Interactions between PMNs and hepatocytes were studied in an ex vivo co-culture model using electron microscopy and lactate dehydrogenase levels. We generated NOD1 antagonist-loaded nanoparticles (np ALINO).NOD1 agonist treatment increased liver injury, PMN tissue infiltration and upregulated ICAM-1 and VCAM-1 expression 20 hours after reperfusion. NOD1 agonist treatment without IR increased expression of adhesion molecules (ICAM-1, VCAM-1) in total liver and more particularly in WT hepatocytes, but not in Nod1 KO hepatocytes. This induction is dependent of p38 and ERK signaling pathways. Compared to untreated hepatocytes, a NOD1 agonist markedly increased hepatocyte lysis in co-culture with PMNs as shown by the increase of lactate dehydrogenase in supernatants. Interaction between hepatocytes and PMNs was confirmed by electron microscopy. In a mouse model of liver IR, treatment with np ALINO significantly reduced the area of necrosis, aminotransferase levels and ICAM-1 expression.NOD1 regulates liver IR injury through induction of adhesion molecules and modulation of hepatocyte-PMN interactions. NOD1 antagonist-loaded nanoparticles reduced liver IR injury and provide a potential approach to prevent IR, especially in the context of liver transplantation.Nucleotide-binding oligomerization domain 1 (NOD1) is as an important modulator of polymorphonuclear neutrophil (PMN)-induced liver injury, which occurs in ischemia-reperfusion. Here, we show that the NOD1 pathway targets liver adhesion molecule expression on the endothelium and on hepatocytes through p38 and ERK signaling pathways. The early increase of adhesion molecule expression after reperfusion emphasizes the importance of adhesion molecules in liver injury. In this study we generated nanoparticles loaded with NOD1 antagonist. These nanoparticles reduced liver necrosis by reducing PMN liver infiltration and adhesion molecule expression.Lire moins >
Lire la suite >In liver transplantation, organ shortage leads to the use of marginal grafts that are more susceptible to ischemia-reperfusion (IR) injury. We identified nucleotide-binding oligomerization domain 1 (NOD1) as an important modulator of polymorphonuclear neutrophil (PMN)-induced liver injury, which occurs in IR. Herein, we aimed to elucidate the role of NOD1 in IR injury, particularly focusing on its effects on the endothelium and hepatocytes.Nod1 WT and KO mice were treated with NOD1 agonists and subjected to liver IR. Expression of adhesion molecules was analyzed in total liver, isolated hepatocytes and endothelial cells. Interactions between PMNs and hepatocytes were studied in an ex vivo co-culture model using electron microscopy and lactate dehydrogenase levels. We generated NOD1 antagonist-loaded nanoparticles (np ALINO).NOD1 agonist treatment increased liver injury, PMN tissue infiltration and upregulated ICAM-1 and VCAM-1 expression 20 hours after reperfusion. NOD1 agonist treatment without IR increased expression of adhesion molecules (ICAM-1, VCAM-1) in total liver and more particularly in WT hepatocytes, but not in Nod1 KO hepatocytes. This induction is dependent of p38 and ERK signaling pathways. Compared to untreated hepatocytes, a NOD1 agonist markedly increased hepatocyte lysis in co-culture with PMNs as shown by the increase of lactate dehydrogenase in supernatants. Interaction between hepatocytes and PMNs was confirmed by electron microscopy. In a mouse model of liver IR, treatment with np ALINO significantly reduced the area of necrosis, aminotransferase levels and ICAM-1 expression.NOD1 regulates liver IR injury through induction of adhesion molecules and modulation of hepatocyte-PMN interactions. NOD1 antagonist-loaded nanoparticles reduced liver IR injury and provide a potential approach to prevent IR, especially in the context of liver transplantation.Nucleotide-binding oligomerization domain 1 (NOD1) is as an important modulator of polymorphonuclear neutrophil (PMN)-induced liver injury, which occurs in ischemia-reperfusion. Here, we show that the NOD1 pathway targets liver adhesion molecule expression on the endothelium and on hepatocytes through p38 and ERK signaling pathways. The early increase of adhesion molecule expression after reperfusion emphasizes the importance of adhesion molecules in liver injury. In this study we generated nanoparticles loaded with NOD1 antagonist. These nanoparticles reduced liver necrosis by reducing PMN liver infiltration and adhesion molecule expression.Lire moins >
Langue :
Anglais
Audience :
Internationale
Vulgarisation :
Non
Établissement(s) :
CHU Lille
Inserm
Institut Pasteur de Lille
Université de Lille
Inserm
Institut Pasteur de Lille
Université de Lille
Collections :
Équipe(s) de recherche :
Therapeutic innovation targetting inflammation
Date de dépôt :
2019-05-17T13:14:49Z
2019-07-08T10:39:09Z
2019-11-12T11:02:30Z
2021-06-09T07:33:18Z
2019-07-08T10:39:09Z
2019-11-12T11:02:30Z
2021-06-09T07:33:18Z
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