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Hsa-miR-200c-3p is down regulated in stable coronary artery disease: A pilot study

ABSTRACT: Four male patients were enrolled for this study in collaboration with the Cardiology Unit of Policlinico Tor Vergata-Fondazione PTV (Rome). The first group of patients has chronic coronary artery disease (CAD) confirmed by coronary angiography, the second group are subjects with clinically proven healthy coronary arteries (CTR). On our case study we have performed a genome-wide methylation study on genomic DNA bisulfite-converted and a miRNA-sequencing study using NextSeq 500 ILLUMINA platform. The methylation study showed different methylated regions (DMRs) and single CpG sites (DMCs) in patients sharing the same clinical and pathological features, allowing detecting distinctly different methylation patterns between CTR subjects and CAD patients. Moreover, miRNA-sequencing results displayed a differential expression of several significant miRNAs (p-value<0.05), defining a peculiar miRNAs profile in patients featuring the same clinical data. miRNA-sequencing and genome-wide methylation integreted results, showed hsa-miR-200c-3p down-regulated in CAD patients compared to control subjects (FC CAD=2.97 and p≤0.05) and with two hypermethylated sites (genomic coordinates: chr12:7073122-7073122 and chr12:7072599-7072599) in its promoter region (p-value=0.009). We extended the validation of these results on all case study (n=96; 24 CTR and 72 CAD).

ORGANISM(S): Homo sapiens

PROVIDER: GSE209779 | GEO | 2025/07/26

REPOSITORIES: GEO

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Project description:Rationale: Epicardial adipose tissue (EAT) has been independently associated with non-calcified, high-risk coronary plaques in low-to intermediate risk subjects. Recently, a bidirectional communication was shown between EAT and diseased coronary arteries. In high-risk patients it is unknown whether quantitative measures of EAT can capture, and which molecular players are involved in this mutual interplay. Objective: In a high-risk population, we aimed to determine how the volume of EAT is linked to coronary artery disease (CAD) and to identify potential EAT-deregulated pathways in CAD patients specifically related to coronary artery calcification (CAC). Methods and Results: In a prospective cohort of 574 degenerative severe aortic stenosis patients referred to cardiac surgery, we quantified fat depots by computed tomography (CT) and performed a comparative quantitative proteomics of thoracic fat, including EAT, mediastinal (MAT) and subcutaneous (SAT) adipose tissues. We did not find an independent association of EAT volume with the severity, distribution and complexity of coronary stenosis in invasive coronary angiography. Although, EAT volume was correlated with high CAC, its cardiovascular risk factors-adjusted association was not significant. Taking as reference non-CAD matched-patients and compared to MAT and SAT, EAT proteomic signature of CAD was characterized by up-regulation of pro-calcifying annexins (Annexin A2, ANXA2), fatty acid binding transporters (FABP4) and inflammatory signaling proteins, and by down-regulation of fetuin-A and redox state regulatory enzymes. In EAT, ANXA2 regulation was positively correlated with CAC. EAT gene expression studies confirmed overexpression of ANXA2 and FABP4 in CAD, but no expression of FETUA was detected. Compared with non-CAD, fetuin-A circulating levels were higher in CAD, whereas no fetuin-A pericardial fluid differences were found. Conclusions: In this high-risk cohort, EAT presented an imbalance of pro-calcifying, pro-inflammatory and lipid transporters mediators. These local EAT-mediated regulatory mechanisms were not reflected by the CT volume of EAT alone.

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Hsa-miR-200c-3p is down regulated in stable coronary artery disease: A pilot study

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