Abstract:
Objective To explore whether the myocardium of newborn SD rats can regenerate after cardiac injury, and screen miRNAs associated with heart repair.
Methods A model of cardiac injury was established in 1-and 2-day-old neonatal SD rats. Fifty rats were divided into two groups, sham group with the chest wall opened and the incision sutured immediately after heart exposure and model group with a little cut-off of the apical tissue, and the rest procedures were the same as the sham group. The model was successfully established in 40 rats with 20 samples in each group and 2 samples were taken as the postoperative 0 day baseline control. Three rats of each group were sacrificed and their hearts were taken and stained with HE and Masson at 7 days and 14 days after operation to observe morphological changes. Four rats of each group were sacrificed and their hearts were taken and expression levels of miRNAs were detected by RT-qPCR at 7 days, 14 days and 21 days after operation. The fold changes of miRNAs at these three time points to those at postoperative 0 day were taken as the relative expression levels. And the expression differences were analyzed between groups at different time points.
Results In the model group, at 7 days after operation, cardiomyocyte degeneration,necrosis and collagen deposition among cardiomyocytes were observed in HE and Masson staining respectively; Scar and myocardial fibrosis had been formed at 14 days. The relative expression of selected 10 miRNAs increased at 7 days after operation, and compared to the sham group, the relative expression of miR-223-3 p was significantly higher in model group(404.28±302.73
vs 6.17±4.61,
P=0.021). The rest miRNAs showed no significant difference between two groups. At 14 days and 21 days after operation, the relative expression levels of all miRNAs showed no significant difference between two groups. During the repair process, miR-223-3 p expression dramatically increased to 404.28 times at 7 days after operation and sharply decreased to 11.85 times at postoperative14 days, which suggested that the change might be closely related to the pathological repair process.
Conclusion The myocardium in neonatal rats can not be completely regenerated after heart injury, and it is mainly repaired by scar and myofibriosis. The increased miR-223-3 p expression indicates that it may be an important regulatory gene for fibrous repair after cardiac injury.