ABSTRACT
BACKGROUND:Recent studies have found that stem cels can directly differentiate into mature myocardial cels or promote their regeneration, providing a new therapeutic strategy for the treatment of myocardial infarction. However, the low cel transplantation rate reduces the myocardial differentiation ability and myocardial repair. OBJECTIVE: To study the role of heat shock treatment in Sca-1+ cel transplantation for treatment of myocardial infarction in mice. METHODS:Sca-1+ cels were isolated from the bone marrow of mice using magnetic bead sorting method, and were subjected to heat shock treatment. Animal models of myocardial infarction were made in mice, and then randomized into two groups: heat shock group and non-heat shock group, which were given 1 mL heat shock-treated Sca-1+ cels and 1 mL non-heat shock-treated Sca-1+ celsvia the tail vein, respectively. After transplantation, cel survival, heart function, myocardial cel apoptosis and myocardial fibrosis were detected. Meanwhile, the expressions of heat shock factor (HSP), HSP70 and miR-34a in the left ventricle were measured. RESULTS AND CONCLUSION:(1) The expression of sry gene in the heat shock group was significantly higher than that in the non-heat shock group. (2) The left ventricular ejection fraction and fractional shortening in the heat shock group were significantly higher than those in the non-heat shock group. The left ventricular end-diastolic diameter and systolic diameter in the heat shock group were significantly lower than those in the non-heat shock group. (3) The cardiac fibrosis and myocardial cel apoptosis in the heat shock group were significantly lower than those in the non-heat shock group. (4) The HSF and HSP70 expression in the left ventricle was significantly higher in the heat shock group than the non-heat shock group, and the miR-34a expression in the left ventricle was significantly lower in the heat shock group than the non-heat shock group. These findings indicate that heat shock-treated Sca-1+ cel transplantation can reduce myocardial apoptosis and infarct size, and improve heart function of mice with myocardial infarction.