Abstract
Stem cells can promote myocardial regeneration and accelerate the formation of new blood vessels. As such, transplanted stem cells represent a promising treatment modality for acute myocardial infarction (AMI). Stem cells spontaneously home to the infarcted myocardium using chemotaxis, in which the stromal cell-derived factor (SDF-1α) has been shown to be one of the most important chemokines. However, spontaneously secreted SDF-1α is short-lived, and therefore does not meet the needs of tissue repair. In this study, adenoviruses carrying SDF-1α genes were loaded on microbubble carriers and the adenoviruses were released into AMI rats by ultrasound targeted microbubble destruction. The possibility of in vivo self-transplantation of bone marrow mesenchymal stem cells (BMSCs) induced by overexpression of SDF-1α in the infarcted myocardium was explored by detecting the number of BMSCs homing from the peripheral blood to the myocardial infarcts. The concentration of SDF-1α in peripheral blood was significantly higher after transfection, and the number of BMSCs was significantly higher in the peripheral blood and infarcted area. Further analyses indicated that the number of homing BMSCs increased with increased SDF-1α expression. In conclusion, our results suggest that ultrasound mediated transduction of exogenous SDF-1α genes into myocardial infarcted AMI rats can effectively promote the homing of endogenous BMSCs into the heart. Moreover, the number of homing stem cells was controlled by the level of SDF-1α expression.
Highlights
Stem cell transplantation in the treatment of acute myocardial infarction (AMI) has become a very promising treatment modality following the results of Hamano [1] and Strauer [2] where bone marrow stem cell transplantation was applied in the successful treatment of myocardial infarction
Our results suggest that ultrasound mediated transduction of exogenous SDF-1α genes into myocardial infarcted AMI rats can effectively promote the homing of endogenous bone marrow mesenchymal stem cells (BMSCs) into the heart
The results indicated that the expression of SDF-1α in AMI rat hearts was successfully induced by ultrasound targeted microbubble destruction (UTMD), and that the expression of SDF-1α increased with time after transfection (Figure 2)
Summary
Stem cell transplantation in the treatment of acute myocardial infarction (AMI) has become a very promising treatment modality following the results of Hamano [1] and Strauer [2] where bone marrow stem cell transplantation was applied in the successful treatment of myocardial infarction. Transplanted bone marrow stem cells (BMSCs) reduce the area of myocardial infarction and promote ischemic cardiac function recovery by promoting myocardial cell regeneration and accelerating neovascularization [3,4,5]. Stem cells can home spontaneously, via chemokine chemotaxis, to the damaged myocardium and become involved in physiological repair. SDF-1α can be secreted spontaneously after a myocardial infarction event, but it can only be maintained for about 4 days. This is a naturally occurring but inefficient repair process in which cells home to myocardial tissue in need of regeneration [14]. A key question remains of how to sustain the expression of SDF-1α in the damaged myocardium
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
