Differences in MicroRNA Expression in Pericoronary Adipose Tissue in Coronary Artery Disease Compared to Severe Valve Dysfunction

Author:

Marketou Maria1ORCID,Kontaraki Joanna2,Kalogerakos Paris3,Plevritaki Anthoula1,Chlouverakis Gregory4,Kassotakis Spyridon1,Maragkoudakis Spyros5,Danelatos Christos1,Zervakis Stelios1,Savva Eirini1,Vardas Panos6,Kochiadakis George1,Lazopoulos George3

Affiliation:

1. Cardiology Department, Heraklion University General Hospital, Crete, Greece

2. Molecular Cardiology Laboratory, School of Medicine, University of CreteUniversity, Crete, Greece

3. Cardiovascular Surgery Department, Heraklion University General Hospital, Crete, Greece

4. Department of Biostatistics, School of Medicine, University of CreteUniversity, Crete, Greece

5. Cardiology Department, Chania General Hospital, Crete, Greece

6. Mitera Hospital, Hygeia Group, Athens, Greece

Abstract

Pericoronary adipose tissue (PCAT) is a source of microRNAs (miRs) that act as messengers for intercellular communication. We investigated whether the PCAT surrounding significant coronary atherosclerotic lesions shows specific miR expression patterns compared with PCAT surrounding plaque-free segments. We included 49 patients with 3-vessel coronary artery disease (CAD) and 19 patients with severe valvular disease but no CAD, who underwent elective cardiac surgery. The PCAT was harvested from two sites: adjacent to a significant atherosclerotic coronary lesion and from plaque-free segments. miR-133a, miR-21, miR-26b, miR-9, and miR-143 levels in PCAT cells were quantified by real-time reverse transcription polymerase chain reaction (data expressed as arbitrary units). Expression of miR-133, miR-21, and miR-26b in adipose tissue at a site without atherosclerotic lesion was much lower in patients with CAD than in those without CAD (0.82 ± 1.37 vs 1.86 ± 0.52, P < .001, 0.45 ± 1.3 vs 1.51 ± 1.11, P < .001, 0.3 ± 1.25 vs 1.2 ± 0.73, P = .02, respectively). In addition, miR-133, miR-21, and miR-143 in CAD patients showed significantly greater expression in PCAT from atherosclerotic lesion compared with plaque-free segments (1.32 ± 0.96 vs 0.82 ± 0.37 (P = .011), 0.91 ± 1.7 vs 0.3 ± 1.25 (P = .012), 1.2 ± 1.59 vs 0.43 ± 0.54 (P < .001), respectively). Our findings open new perspectives for the role of PCAT in the pathophysiology of atherosclerosis and should be further investigated.

Funder

Hellenic Society of Cardiology

Publisher

SAGE Publications

Subject

Cardiology and Cardiovascular Medicine

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