MICRORNA PROFILE ANALYSIS IN PERICORONARY ADIPOSE TISSUE OF DIABETIC PATIENTS WITH SIGNIFICANT CORONARY ARTERY DISEASE

Objective: Pericoronary adipose tissue (PCAT) regulates arterial homeostasis, is considered to act in paracrine manner, and plays a role in the pathogenesis of atherosclerosis. PCAT may be a source of microRNAs (miRs) that target other tissues and act as messengers for intercellular communication. We investigated whether the PCAT surrounding coronary occlusive atherosclerotic lesions shows specific miRs expression patterns in patients with diabetes type 2 compared to non-diabetic patients. Design and method: We enrolled 51 patients (35 men, aged 67±12 years old) with 3-vessel coronary artery disease who underwent elective coronary bypass surgery with and without diabetes type 2. The PCAT samples were received from all participants. miR-133a, miR-26b, miR-9 and miR-143 expression levels in PCAT cells were quantified by real-time reverse transcription polymerase chain reaction. Results: Twenty-seven patients with diabetic type 2 (16 men, 66 ± 10 years old) and twenty-four non-diabetic patients (15 men, 67 ± 15 years old) were included in the study. Diabetic patients also revealed a significant increase of miR-26b and miR-143 expression in PCAT samples compared to the non-diabetic group (36 ± 20 versus 16 ±17, p = 0.02, 99±45 versus 19 ± 27, p = 0.01). No significant differences between the two groups were observed in PCAT expression of miR-133a and miR-9 (83± 22 versus 111 ±146, 56±49 versus 39 ± 33, respectively, p =NS for both). Notably, the expression of miR-143 and miR-26b in PCAT from atherosclerotic plaque showed robust positive correlations with BMI of total population (r = 0.451, p = 0.001 and r=0.41, p = 0.03 respectively). Conclusions: miRs expression in PCAT from diabetic patients with significant coronary disease show a distinct expression profile. Our study opens new perspectives in the pathophysiologic role of PCAT in atherosclerotic complications of diabetes and should be further investigated.