Abstract

0bjective Comparison of bone marrow stem cells (BMSCs) transplantation and sarcoplasmic reticulum Ca 2+ -ATPase (SERCA2a) gene modified BMSCs transplantation for therapy effects after acute myocardial infarction(AMI), as well as for assessment cardiac electrical activity by microelectrode array (MEA) technology. Methods Rats with myocardial infarction ( n =24)and divided into 3 groups randomly: Sham group ( n =8), BMSCs group( n =8) and SERCA2a gene modified BMSCs transplantation group (BMSCs+rAd.SERCA2a group, n =8). After 14 days, cardiac function was evaluated by echocardiography and heart electrical activity was evaluated by electrocardiogram and MEA technology. Results (1)The transduction ration of rAd.SERCa2a to BMSCs were 80% to 90%. (2)Compared to sham group, BMSCs group and BMSCs+rAd.SERCA2a group could significantly improve cardiac function on 14 days after therapy ( n =6, P <0.05).(3)QT duration of BMSCs+rAd.SERCA2a group was significantly shorter than in the sham group(80.30 ms±6.53 ms versus 105.31 ms±21.89 ms),the mean value was significantly decreased 23.8%( n =7, P <0.05). Ventricular premature beats were also recorded in rats from sham group.(4)MEA results suggested that isolated heart beats were significantly slowed and ventricular arrhythmias and atrioventrocular block were recorded in sham group. The maximum field potential and field potential duration of infarcted myocardium area in BMSCs group and BMSCs+rAd.SERCA2a group were significantly longer than those in sham group(the maximum field potential: 0.51 mV±0.15 mV, 0.55 mV±0.16 mV, 0.23 mV±0.1mV; field potential duration: 104.5 ms±25.43 ms, 107.67 ms ±24.01 ms, 63 ms± 20.34 ms; n =6, P <0.05).(5)The conduction time was the shortest in BMSCs+rAd.SERCA2a group, the cardiac electrical conduction could keep consistency and improve in myocardial infarction tissue. Conclusions In short time, BMSCs and SERCA2a gene modified BMSCs transplantation could obviously enhance cardiac function. BMSCs+rAd.SERCA2a group could effectively improve electrical conduction of infarcted myocardium and block the occurrence of arrhythmia after myocardial infarction.

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