Journal
CARDIOVASCULAR RESEARCH
Volume 109, Issue 2, Pages 228-239Publisher
OXFORD UNIV PRESS
DOI: 10.1093/cvr/cvv266
Keywords
Epicardial adipose tissue; Gene expression; miRNA; Metabolic syndrome; Nuclear receptors
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Funding
- NR-NET FP7 Marie Curie ITN
- Italian Ministry of University and Education [RBID08C9N7, PON01_01958, PRIN 2010FHH32M-002, PRIN 20085Y7XT5_004]
- Italian Ministry of Health [GR-2008-1143546, GR-2010-2314703]
- Apulian Region (POR Strategic Projects) [CIP PS_101]
- University of Bari, Italy [ORBA 08WEZJ, 07X7Q1, 06BXVC, IDEA GRBA0802SJ]
- Fondazione 'Umberto Veronesi' (fellowship)
- Medical Research Council (MRC-HNR) [MC_PC_13030]
- MRC [MC_PC_13030, MR/P011705/1, MR/P01836X/1] Funding Source: UKRI
- Associazione Italiana per la Ricerca sul Cancro Funding Source: Custom
- Medical Research Council [MC_PC_13030, MR/P01836X/1, MR/P011705/1] Funding Source: researchfish
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Background Epicardial adipose tissue (EAT) is an atypical fat depot surrounding the heart with a putative role in the development of atherosclerosis. Methods and results 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. Conclusion EAT in CADis 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.
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