Comparative Evaluation of Immunophenotype and Expression Level of Osteogenic Differentiation Genes in Mesenchymal Stem Cells from Epicardial and Subcutaneous Adipose Tissue in Coronary Heart Disease

Coronary artery calcification (CAC) is an important factor in the pathogenesis of coronary heart disease. Mesenchymal stem cells in epicardial adipose tissue (EAT MSCs) may represent an active cellular component contributing to the development of vascular calcification, although their role in the pathogenesis of CAC remains unexplored. Assessing the immunophenotypic features and osteoblastic potential of EAT MSCs compared to MSCs from subcutaneous adipose tissue (SAT MSCs) will allow a deeper insight into the cellular processes leading to calcium deposition in the coronary arteries. MSC immunophenotype was identified using flow cytometry. Expression levels of MSC surface antigens CD90, CD31, CD45, CD73, CD105, and HLA-DR were measured. To determine the expression levels of osteogenic differentiation genes RUNX2 , BGLAP , ALPL , SPP1 , MSC cultures derived from EAT and SAT were studied on days 3, 15, and 21 using real-time PCR. To assess osteogenic efficiency, the cultures were stained with a calcium-tropic dye, and calcium concentration was measured photometrically. Both EAT and SAT MSCs obtained from patients with coronary heart disease carried CD73, CD105, and CD90 antigens on their surface, although the proportion of CD73- and CD90-positive cells in the culture of EAT MSCs was 3 and 1.3 times lower, respectively, than in that of SAT MSCs. The expression profile of osteogenic genes in EAT MSCs showed that this culture has a greater osteogenic potential compared to SAT MSCs, as confirmed by a relatively high expression of RUNX2 , SP7 , BGLAP , ALPL , SPP1 genes in the culture of epicardial MSCs. Conclusions: MSCs derived from EAT exhibit a higher osteogenic potential compared to MSCs derived from SAT. This may play a key role in the pathogenesis of coronary artery calcification in patients with coronary heart disease.