Interleukin-33/ST2 system attenuates aldosterone-induced adipogenesis and inflammation.
Fiche publication
Date publication
août 2015
Journal
Molecular and cellular endocrinology
Auteurs
Membres identifiés du Cancéropôle Est :
Pr ROSSIGNOL Patrick
Tous les auteurs :
Martínez-Martínez E, Cachofeiro V, Rousseau E, Álvarez V, Calvier L, Fernández-Celis A, Leroy C, Miana M, Jurado-López R, Briones AM, Jaisser F, Zannad F, Rossignol P, López-Andrés N
Lien Pubmed
Résumé
Interleukin-33 (IL-33) but not soluble ST2 (sST2) exerts anti-inflammatory and protective effects in several tissues. Aldosterone, a proinflammatory mediator which promotes adipogenesis, is elevated in obese patients. The aim of this study was to investigate the interactions between IL-33/ST2 system and Aldosterone in adipose tissue. Rats fed a high fat diet presented increased sST2 expression, diminished IL-33/sST2 ratio and enhanced levels of differentiation and inflammation in adipose tissue as compared to controls. A similar pattern was observed in adipose tissue from C57BL/6 Aldosterone-treated mice. In both animal models, Aldosterone was correlated with sST2. Treatment of 3T3-L1 adipocytes with IL-33 delayed adipocyte differentiation diminished lipid accumulation and decreased inflammation. Aldosterone decreased IL-33 and increased sST2 expressions in differentiated adipocytes. Aldosterone-induced adipocyte differentiation and inflammation were blocked by IL-33 treatment, but sST2 did not exert any effects. The crosstalk between IL-33/ST2 and Aldosterone could be relevant in the metabolic consequences of obesity.
Mots clés
3T3-L1 Cells, Adipogenesis, drug effects, Adipose Tissue, drug effects, Aldosterone, pharmacology, Animals, Diet, High-Fat, Inflammation, metabolism, Interleukin-1 Receptor-Like 1 Protein, Interleukin-33, metabolism, Male, Mice, Mice, Inbred C57BL, Obesity, metabolism, Rats, Rats, Wistar, Receptors, Interleukin, metabolism
Référence
Mol. Cell. Endocrinol.. 2015 Aug 15;411:20-7