Interferon-gamma induced adipose tissue inflammation is linked to endothelial dysfunction in type 2 diabetic mice
- نوع فایل : کتاب
- زبان : انگلیسی
- مؤلف : Hanrui Zhang , Barry J. Potter , Ji-Min Cao , Cuihua Zhang
- چاپ و سال / کشور: 2011
Description
Interferon-gamma (IFNc) has previously been associated with immuno-mediated inflammation in dietinduced obesity and type 1 diabetes. This study sought to define the role of IFNc-induced adipose tissue inflammation in endothelial dysfunction in type 2 diabetes. We examined mesenteric adipose tissue (MAT) inflammation, and endothelial function of small mesenteric artery (SMA) in control mice (m Leprdb), diabetic mice (Leprdb), m Leprdb treated with IFNc, and Leprdb treated with anti-IFNc or anti-monocyte chemoattractant protein-1 (anti-MCP-1). mRNA and protein expression of IFNc and MCP-1 were increased in MAT of Leprdb, accompanied by increased T-lymphocyte and macrophage infiltration. Anti-IFNc reduced MAT inflammatory cell infiltration and inflammatory cytokine expression in Leprdb, while IFNc treatment showed the opposite effects in m Leprdb. Acetylcholine (ACh)-induced vasorelaxation of SMA was impaired in Leprdb versus m Leprdb, but sodium nitroprusside (SNP)-induced vasorelaxation was comparable. Both anti-IFNc and anti-MCP-1 improved endothelial function of Leprdb, while IFNc treatment impaired endothelial function of m Leprdb. Superoxide production was higher in both MAT and SMA of Leprdb mice, and anti- IFNc reduced MAT and SMA superoxide production. Macrophage accumulation in the adventitia of SMA, and mRNA expression of MCP-1 in SMA were increased in Leprdb and IFNc-treated m Leprdb, but reduced in anti- IFNc treated Leprdb. These findings suggest IFNc has a key role in the regulation of visceral adipose tissue inflammatory response and endothelial dysfunction in type 2 diabetes
Basic Res Cardio lReceived: 21 March 2011 / Revised: 24 June 2011 / Accepted: 28 July 2011
