Investigation of the microRNA signatures and their potential role in pathomechanism of coronary artery disease and aortic valve disease

Investigation the role of microRNA signatures in coronary artery disease and aortic valve disease

Background: Coronary artery disease (CAD) and aortic valve disease (AVD) are significant cardiovascular conditions with complex pathogenesis, involving processes such as inflammation, smooth muscle cell proliferation, and endothelial dysfunction. Recent studies have identified microRNAs (miRNAs) as key regulators of gene expression in cardiovascular diseases, impacting disease progression. This study focuses on the roles of miR-210, miR-92a, and miR-122, exploring their regulatory functions and potential as biomarkers in CAD and AVD. Human coronary artery endothelial cells (HCAEC) and human coronary artery smooth muscle cells (HCASMC) were utilized as in vitro models to mimic cellular responses under disease conditions.

Methods: Serum samples were collected from patients with CAD and AVD, and miRNAs were extracted to measure expression levels of miR-210, miR-92a, and miR-122 via quantitative real-time PCR (qRT-PCR). Additionally, HCAEC and HCASMC were transfected with each of these miRNAs to assess their effects on cell proliferation, migration, and inflammatory responses. The observed changes in cellular behavior were analyzed to understand the regulatory role of these miRNAs in vascular pathology.

Results: Preliminary data indicated that miR-210 and miR-92a are significantly upregulated in CAD and AVD patients, suggesting potential roles in endothelial and inflammatory regulation. In vitro experiments showed that overexpression of miR-210 and miR-92a markedly enhanced HCAEC and HCASMC proliferation and migration. In contrast, miR-122 expression was significantly downregulated in AVD patients, and in smooth muscle cells, it appeared to inhibit migration and proliferation. These findings suggest that while miR-210 and miR-92a may act as promoters of disease progression in CAD and AVD, miR-122 may have a protective function.

Conclusion: This study demonstrates the distinct roles of miR-210, miR-92a, and miR-122 in the progression of CAD and AVD. The upregulation of miR-210 and miR-92a likely contributes to increased proliferation and migration of endothelial and smooth muscle cells, potentially accelerating disease progression, whereas the downregulation of miR-122 might reduce its protective effects. These miRNAs hold promise as diagnostic and therapeutic biomarkers for CAD and AVD.