Improved systolic function of rat cardiocytes during heart failure by overexpression of SERCA2a

This study shows that overexpression of SERCA2a can improve the systolic function and reduce the occurr-ence of arrhythmias in cardiocytes isolated from the heart of a rat model of heart failure.

An animal model of rats experiencing heart failure was established by a surgical procedure producing abdominal aortic coarctation. Cardiocytes from sacrificed rats were isolated by a collagenase digestion method. The SERCA2a adenovirus vector was transfected into the cells after 48h of culture. Overexpression of SERCA2a in cardiocytes was verified by Western Blot. Measurements were taken using a single cell dynamic edge detection system to evaluate the effects on the myocardiocyte function and calcium homeostasis.

Cardiocytes overexpressing SERCA2a displayed a stronger systolic function and lower occurrence rate of abnormal systolic rhythm than mock-transfected cardiocytes. The contraction rhythm abnormality rate percentage was 5.270 ± 1.566% vs. 3.955 ± 1.684% (p < 0.01). The time at which they reached the maximum contraction (TTP) was 0.095 ± 0.009s vs. 0.114 ± 0.008s (p < 0.01). The time at which they reached 50% of the diastolic amplitude (R50) was 0.039 ± 0.008s vs. 0.057 ± 0.010s (p < 0.01). Finally, the occurrence rate of abnormal systolic rhythm during maximal contraction was 58% vs. 81% (p < 0.01). These results show that all data were significantly improved in the SERCA2a overexpressing group, and that parameters achieved were similar to those in the sham-operated non-heart failure group.

The overexpression of SERCA2a in cardiocytes during heart failure significantly improves cell function and arrhythmia occurrence.