4.7 Article

Integrative miRNA and whole-genome analyses of epicardial adipose tissue in patients with coronary atherosclerosis

期刊

CARDIOVASCULAR RESEARCH
卷 109, 期 2, 页码 228-239

出版社

OXFORD UNIV PRESS
DOI: 10.1093/cvr/cvv266

关键词

Epicardial adipose tissue; Gene expression; miRNA; Metabolic syndrome; Nuclear receptors

资金

  1. NR-NET FP7 Marie Curie ITN
  2. Italian Ministry of University and Education [RBID08C9N7, PON01_01958, PRIN 2010FHH32M-002, PRIN 20085Y7XT5_004]
  3. Italian Ministry of Health [GR-2008-1143546, GR-2010-2314703]
  4. Apulian Region (POR Strategic Projects) [CIP PS_101]
  5. University of Bari, Italy [ORBA 08WEZJ, 07X7Q1, 06BXVC, IDEA GRBA0802SJ]
  6. Fondazione 'Umberto Veronesi' (fellowship)
  7. Medical Research Council (MRC-HNR) [MC_PC_13030]
  8. MRC [MC_PC_13030, MR/P011705/1, MR/P01836X/1] Funding Source: UKRI
  9. Associazione Italiana per la Ricerca sul Cancro Funding Source: Custom
  10. Medical Research Council [MC_PC_13030, MR/P01836X/1, MR/P011705/1] Funding Source: researchfish

向作者/读者索取更多资源

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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