Human umbilical cord blood-mesenchymal stem cell-derived secretome in combination with atorvastatin enhances endothelial progenitor cells proliferation and migration

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.

Different Inhibition Mechanism of Atorvastatin, Olmesartan, and Resveratrol in Experimental Pathological Myofibroblast Heart Valve Model

“…The expression of 𝛼 -SMA indicates the transition from valvular interstitial cells to myofibroblasts, followed by excessive production of inflammatory mediators, growth factors, and synthesis of extracellular matrix of collagen and fibronectin [27]. A number of research [27][28][29][30] have found that statins reduce left ventricular hypertrophy and cardiac fibrosis in hypertension and coronary artery disease. However, statin benefits in valvular interstitial cell fibrosis models has remained elusive [31].…”

Inhibition of Pathological Myofibroblast Differentiation of Valvular Interstitial Cell by Atorvastatin, Olmesartan, and Resveratrol in Experimental Heart Valve Model “Contemporary Model with Rabbit Valve”

“…A number of research [25][26][27][28] have found that statins reduce left ventricular hypertrophy and cardiac brosis in hypertension and coronary artery disease. However, statin bene ts in valvular interstitial cell brosis models has remained elusive [29].…”

Inhibition of Pathological Myofibroblast Differentiation of Valvular Interstitial Cell by Atorvastatin, Olmesartan, and Resveratrol in Experimental Heart Valve Model “Contemporary Model with Rabbit Valve”

“…A number of research [25][26][27][28] have found that statins reduce left ventricular hypertrophy and cardiac fibrosis in hypertension and coronary artery disease. However, statin benefits in valvular interstitial cell fibrosis models has remained elusive [29].…”