Abstract
Background: Human umbilical cord blood-mesenchymal stem cell (hUCB-MSC)-derived secretome is known to be able to promote neovascularization and angiogenesis, so it is also thought to have a capability to modulate endothelial progenitor cell (EPC) functions. Atorvastatin is the cornerstone of coronary artery disease (CAD) treatment which can enhance EPCs proliferation and migration. This study aims to analyze the effect of the hUCB-MSC-derived secretome and its combination with atorvastatin toward EPCs proliferation and migration. Methods: EPCs were isolated from a CAD patient's peripheral blood. Cultured EPCs were divided into a control group and treatment group of 2.5 µM atorvastatin, hUCB-MSC-derived secretome (2%, 10%, and 20% concentration) and its combination. EPCs proliferation was evaluated using an MTT cell proliferation assay, and EPC migration was evaluated using a Transwell migration assay kit. Results: This research showed that hUCB-MSC-derived secretomes significantly increase EPC proliferation and migration in a dose-dependent manner. The high concentration of hUCB-MSC-derived secretome were shown to be superior to atorvastatin in inducing EPC proliferation and migration (p<0.001). A combination of the hUCB-MSC-derived secretome and atorvastatin shown to improve EPCs proliferation and migration compared to hUCB-MSC-derived secretome treatment or atorvastatin alone (p<0.001). Conclusions: This study concluded that the hUCB-MSC-derived secretome work synergistically with atorvastatin treatment in improving EPCs proliferation and migration.
Highlights
Coronary artery disease (CAD) is the leading cause of mortality and morbidity worldwide1
This study aims to compare the effect of the hUCB-mesenchymal stem cells (MSCs)-derived secretome, atorvastatin and the two in combination in modulating endothelial progenitor cell (EPC) proliferation and migration
It was confirmed through light microscopy that displayed a spindle-shape morphology, which is typical for early EPCs and an immunofluorescence assay that showed FITC CD 34+ expression (Figure 1)
Summary
Coronary artery disease (CAD) is the leading cause of mortality and morbidity worldwide. Coronary artery disease (CAD) is the leading cause of mortality and morbidity worldwide1 It is responsible for the deaths of 7.2 million people or 12.2% of total deaths per year worldwide. Atorvastatin is the cornerstone of coronary artery disease (CAD) treatment which can enhance EPCs proliferation and migration. This study aims to analyze the effect of the hUCB-MSC-derived secretome and its combination with atorvastatin toward EPCs proliferation and migration. Cultured EPCs were divided into a control group and treatment group of 2.5 μM atorvastatin, hUCB-MSC-derived secretome (2%, 10%, and 20% concentration) and its combination. The high concentration of hUCB-MSC-derived secretome were shown to be superior to atorvastatin in inducing EPC proliferation and migration (p
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