Indoleamine 2 3-dioxygenase knockout limits angiotensin II-induced aneurysm in low density lipoprotein receptor-deficient mice fed with high fat diet.
Fiche publication
Date publication
mars 2018
Journal
PloS one
Auteurs
Membres identifiés du Cancéropôle Est :
Dr POTTEAUX Stéphane
Tous les auteurs :
Metghalchi S, Vandestienne M, Haddad Y, Esposito B, Dairou J, Tedgui A, Mallat Z, Potteaux S, Taleb S
Lien Pubmed
Résumé
Abdominal aortic aneurysm (AAA) is an age-associated disease characterized by chronic inflammation, vascular cell apoptosis and metalloproteinase-mediated extracellular matrix degradation. Despite considerable progress in identifying targets involved in these processes, therapeutic approaches aiming to reduce aneurysm growth and rupture are still scarce. Indoleamine 2-3 dioxygenase 1 (IDO) is the first and rate-limiting enzyme involved in the conversion of tryptophan (Trp) into kynurenine (Kyn) pathway. In this study, we investigated the role of IDO in two different models of AAA in mice.
Mots clés
Angiotensin II, adverse effects, Animals, Aortic Aneurysm, Abdominal, chemically induced, Apoptosis, Cell Survival, Cells, Cultured, Diet, High-Fat, adverse effects, Disease Models, Animal, Indoleamine-Pyrrole 2,3,-Dioxygenase, deficiency, Macrophages, cytology, Male, Mice, Mice, Knockout, Muscle, Smooth, Vascular, cytology, Myocytes, Smooth Muscle, cytology, Receptors, LDL, deficiency, T-Lymphocytes, cytology
Référence
PLoS One. 2018 03 1;13(3):e0193737