Objective: To investigate the feasibility of constructing sick sinus syndrome disease model in miR-5572 transgenic mice.
Methods: The F1 and F2 generation wild type homozygous and heterozygous mice of miR-5572 were bred and identified, and the disease model was observed by morphology, ECG recording and determination of Cav1.2, Cav1.3 mRNA and protein expression levels in sinus node tissues.
Results: The F2 generation miR-5572 homozygous knockout mice grew slower and smaller than the wild type mice in morphology. Compared with heterozygous and wild type mice, the average heart rate of homozygous mice was significantly lower (P<0.05). The expression levels of Cav1.2, Cav1.3 mRNA and protein in sinoatrial node tissues of miR-5572 homozygous mice were lower than those of wild type mice (P<0.05).
Conclusion: Transgenic mice overexpressing miR-5572 can construct sick sinus syndrome disease model.