Abstract
Circulating endothelial progenitor cells (cEPCs) are having involvement in the replacing vascular endothelial cells damaged or detachment from the basement membrane. cEPC needs to fulfill both quantity and quality requirements in order to play this important role. After efflux from bone marrow to circulation, niche EPC necessary of maturation to reach the potential for re-endothelialization. Risk factors exposure for cardiovascular disease not only affect the quantity and quality of cEPC, but it is also to be involved in downregulation of SIRT1. SIRT1 downregulation is mostly associated with the mechanism of senescence. Objective. to predict the direction of SIRT-1 interaction with cEPC maturation that is validated with cEPC marker surface using the STRING DB method of protein interaction. Result. SIRT1 interacts with two proteins, inhibiting VEGFA and activating and inhibiting P53. P53 inhibits the expression of p16ink4a, a protein involved in cellular senessence and P53 through AKT involved in CD 309 and ITGA2B expression. Whereas there was a direct interaction of the expression of CD 309 through the VEGFA line; CD117; TIE-2; CD 144; CD62a. Conclusion. SIRT-1 is an intracellular protein that is involved in cellular anti-aging processes but is not directly involved in the expression of EPC marker surfaces.
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