Abstract
Background: Myocardial infarction (MI) is a fatal disease that is increasing in incidence. The worst sequelae of MI include myocardial fibrosis and deterioration of pumping function that can lead to irreversible heart failure. This study aims to compare the therapeutic effect of undifferentiated versus TGF-β2–stimulated Wharton’s jelly mesenchymal stem cells (WJ-MSCs) in MI rats. Results: Left anterior descending (LAD) artery ligation-induced myocardial infarct rats were used to evaluate changes in left ventricular function and fibrosis following injection of PBS or 1.6 × 106 undifferentiated or TGF-β2–stimulated WJ-MSCs into the border zone myocardium. Electrocardiograph, echocardiogram, serum cardiac Troponin I level, Masson’s Trichrome staining, immunohistochemistry were used to analyze the therapeutic effects. We found that transplantation of both undifferentiated and TGF-β2 stimulated WJ-MSCs decreased serum Cardiac Troponin I levels, improved fractional shortening, ameliorated ejection fraction changes, and decreased the area of myocardial fibrosis. Moreover, some of the transplanted human WJ-MSCs survived in the myocardium. Conclusions: Transplantation of either undifferentiated or TGF-β2 stimulated WJ-MSCs improved left ventricular function after MI and increased survival. The effects were most marked using undifferentiated WJ-MSCs. These results indicate WJMSCs as a potential stem cell source for use in myocardial infarct therapy.
Highlights
Myocardial infarction (MI) is a fatal disease that is increasing in incidence
The immunofluorescence staining of the cardiogenic differentiation marker, such as c-Troponin-I and connexin-43 were found to highly expression in the TGF-β2 stimulated Wharton’s jelly mesenchymal stem cells (WJ-Mesenchymal stems cells (MSCs)), confirming that 6 days TGF-β2 treatment induced cardiomyocyte differentiation (Figure 1)
ECG will show ST elevation followed by ST depression or T-wave inversion
Summary
Myocardial infarction (MI) is a fatal disease that is increasing in incidence. The worst sequelae of MI include myocardial fibrosis and deterioration of pumping function that can lead to irreversible heart failure. Myocardial infarction is an ischemic heart condition caused by occlusion of a coronary artery. The occlusion most commonly occurs in the left anterior descending branch of the coronary artery. Injury of myocardiocytes and subsequent heart failure can occur 20–30 minutes after the onset of cardiac ischemia [13]. Healthy myocardiocytes must increase their contractile force to compensate for dead cells to maintain normal pumping. This compensation leads to a vicious cycle whereby compensatory mechanisms proceed to accelerate cardiac hypertrophy [5]
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