Abstract
Background: It is postulated that an impairment of mitochondrial energy-producing ability may lead to the development of chronic heart failure (CHF) following acute myocardial infarction (AMI). In this study, effects of c-Kit- or Sca-1-positive cardiac progenitor cells transplantation to the cardiac tissue after AMI on the cardiac mitochondrial energy-producing ability were examined.
Methods: c-Kit- or Sca-1-positive cells were isolated from adult rat hearts by magnetic cell sorting method, respectively. AMI was induced by ligation of the left ventricular coronary artery in Wistar male rats. Immediately after coronary artery ligation (CAL), approximately 1 million c-Kit- or Sca-1-positive cells were injected into viable myocardium.
Results: Eight weeks after CAL, animals without transplantation showed signs of CHF such as impairment of cardiac pump function. Furthermore, the mitochondrial oxygen consumption rate (mtOCR) of the viable cardiac tissue in rats with CHF was reduced. In contrast, the cardiac pump function and mtOCR were preserved without reduction of infarct size in CAL animals with transplantation of c-Kit- or Sca-1-positive cells.
Conclusions: These results suggest that the transplantation of c-Kit- or Sca-1-positive cells into the infarcted rat heart contributes to a preservation of mitochondrial function, leading to an improvement of cardiac contractile function without regeneration of cardiac tissues.
