Interleukin-33/ST2 system attenuates aldosterone-induced adipogenesis and inflammation. (15th August 2015)

• Record Type: Journal Article
• Authors: Martínez-Martínez, Ernesto; Cachofeiro, Victoria; Rousseau, Elodie; Álvarez, Virginia; Calvier, Laurent; Fernández-Celis, Amaya; Leroy, Céline; Miana, María; Jurado-López, Raquel; Briones, Ana M.; Jaisser, Frederic; Zannad, Faiez; Rossignol, Patrick; López-Andrés, Natalia
• Is Part Of: Molecular and cellular endocrinology. Volume 411(2015)
• Page Start: 20
• Page End: 27
• Publication Date: 2015-08-15
• Subjects: Adipocyte differentiation -- Adipose tissue -- Aldosterone -- IL-33/ST2 system; Endocrinology -- Periodicals; Molecular biology -- Periodicals; Cytology -- Periodicals; Endocrinology -- Periodicals; Hormones -- Periodicals; Endocrinologie -- Périodiques; Cytology; Endocrinology; Molecular biology; Periodicals; 573.4
• DOI: 10.1016/j.mce.2015.04.007
• Languages: English
• ISSNs: 0303-7207

Abstract

Highlights: Aldosterone and sST2 are associated in pathological conditions such as obesity. Obesity and Aldosterone increase deleterious sST2 in adipocytes. Obesity and Aldosterone decrease IL-33/ST2L protective activity in adipocytes. IL-33 blocks Aldosterone-induced adipocyte differentiation and inflammation. IL-33 could attenuate metabolic disorders associated to Aldosterone excess. Abstract: 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.