TY - JOUR
T1 - Integrative miRNA and whole-genome analyses of epicardial adipose tissue in patients with coronary atherosclerosis
AU - Vacca, Michele
AU - Di Eusanio, Marco
AU - Cariello, Marica
AU - Graziano, Giusi
AU - D'Amore, Simona
AU - Petridis, Francesco Dimitri
AU - D'Orazio, Andria
AU - Salvatore, Lorena
AU - Tamburro, Antonio
AU - Folesani, Gianluca
AU - Rutigliano, David
AU - Pellegrini, Fabio
AU - Sabbà, Carlo
AU - Palasciano, Giuseppe
AU - Di Bartolomeo, Roberto
AU - Moschetta, Antonio
N1 - Publisher Copyright:
© 2015 Published on behalf of the European Society of Cardiology. All rights reserved The Author 2015.
PY - 2016/2/1
Y1 - 2016/2/1
N2 - 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 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.
AB - 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 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.
KW - Epicardial adipose tissue
KW - Gene expression
KW - Metabolic syndrome
KW - Nuclear receptors
KW - miRNA
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U2 - 10.1093/cvr/cvv266
DO - 10.1093/cvr/cvv266
M3 - Article
C2 - 26645979
AN - SCOPUS:84959867280
SN - 0008-6363
VL - 109
SP - 228
EP - 239
JO - Cardiovascular Research
JF - Cardiovascular Research
IS - 2
ER -