Vacca Michele, Di Eusanio Marco, Cariello Marica, Graziano Giusi, D'Amore Simona, Petridis Francesco Dimitri, D'orazio Andria, Salvatore Lorena, Tamburro Antonio, Folesani Gianluca, Rutigliano David, Pellegrini Fabio, Sabbà Carlo, Palasciano Giuseppe, Di Bartolomeo Roberto, Moschetta Antonio
Department of Interdisciplinary Medicine, University of Bari 'Aldo Moro', Piazza Giulio Cesare 11, 70124 Bari, Italy Fondazione Mario Negri Sud, Santa Maria Imbaro (CH), Italy Ageing Research Center (CeSI), 'G. d'Annunzio' University Foundation, Chieti, Italy.
Cardiovascular Department, 'S.Orsola Malpighi' Hospital, University of Bologna, Bologna, Italy.
Cardiovasc Res. 2016 Feb 1;109(2):228-39. doi: 10.1093/cvr/cvv266. Epub 2015 Dec 8.
Epicardial adipose tissue (EAT) is an atypical fat depot surrounding the heart with a putative role in the development of atherosclerosis.
We profiled genes and miRNAs in perivascular EAT and subcutaneous adipose tissue (SAT) of metabolically healthy patients without coronary artery disease (CAD) vs. metabolic patients with CAD. Compared with SAT, a specific tuning of miRNAs and genes points to EAT as a tissue characterized by a metabolically active and pro-inflammatory profile. Then, we depicted both miRNA and gene signatures of EAT in CAD, featuring a down-regulation of genes involved in lipid metabolism, mitochondrial function, nuclear receptor transcriptional activity, and an up-regulation of those involved in antigen presentation, chemokine signalling, and inflammation. Finally, we identified miR-103-3p as candidate modulator of CCL13 in EAT, and a potential biomarker role for the chemokine CCL13 in CAD.
EAT in CAD is characterized by changes in the regulation of metabolism and inflammation with miR-103-3p/CCL13 pair as novel putative actors in EAT function and CAD.
心外膜脂肪组织(EAT)是围绕心脏的一种非典型脂肪库,在动脉粥样硬化的发展中可能发挥作用。
我们分析了无冠状动脉疾病(CAD)的代谢健康患者与患有CAD的代谢患者的血管周围EAT和皮下脂肪组织(SAT)中的基因和微小RNA(miRNA)。与SAT相比,miRNA和基因的特定调节表明EAT是一种具有代谢活跃和促炎特征的组织。然后,我们描绘了CAD中EAT的miRNA和基因特征,其特征是参与脂质代谢、线粒体功能、核受体转录活性的基因下调,以及参与抗原呈递、趋化因子信号传导和炎症的基因上调。最后,我们确定miR-103-3p是EAT中CCL13的候选调节因子,并且趋化因子CCL13在CAD中具有潜在的生物标志物作用。
CAD中的EAT具有代谢和炎症调节变化的特征,miR-103-3p/CCL13对是EAT功能和CAD中新型的潜在作用因子。