INHIBITION OF WNT3A DIMINISHED ANGIOGENIC DIFFERENTIATION CAPACITY OF RAT CARDIAC PROGENITOR CELLS

Myocardial infarction is a leading cause of human mortality in industrialized and developing societies. Limited restorative ability of of cardiomyocytes after ischemic changes can causes extensive damage lead to prominent chronic heart failure. At present, the application of certain drugs is touted as one of the main available approaches to inhibit the spread of the lesion and to maintain the integrity of the myocardial tissue after infarction. Today, the transplantation of stem cells to restore structure and maintain heart function has opened new hopes for clinicians in human medicine. These cells accelerate the healing process by secreting a variety of factors and differentiation into varient cell lines, including vascular cells. Here, we investigated the inhibitory role of Wnt3a factor on the process of differentiation of rat cardiomyoblast (H9C2) to endothelial cells.  

In this experimental study, rat cardiomyoblast (H9C2) were expanded in DMEM/HG and exposed to 10 µM LGK-974 (a Wnt3a inhibitor) for 48 hours. The viability of cells was determined using MTT method. The ability to differentiation into endothelial cells was assessed by measuring expression and protein levels of VE-Cadherin and vWF using real-time PCR and western blotting. 

The inhibition of Wnt3a in H9C2 cells could significantly reduce cell survival rate after 48 hours compared to the control cells (p<0.05). Based on data, expression and protein levels of VE-Cadherin and vWF were significantly diminished in group incubated with LGK-974

The inhibition of Wnt3a can suppress the angiogenic potential of rat cardio myoblasts