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As a single cardiac malformation, ventricular septal defect (VSD) is the most common form of congenital heart disease. However, the precise molecular mechanisms underlying VSD are not completely understood. Numerous microRNAs (miRs/miRNAs) are associated with ventricular septal defects. miR-29c inhibits the proliferation and promotes the apoptosis and differentiation of P19 embryonal carcinoma cells, possibly via suppressing Wnt4 signaling. However, to the best of our knowledge, no in&amp;nbsp;vivo studies have been published to determine whether overexpression of miR-29c leads to developmental abnormalities. The present study was designed to observe the effect of miRNA-29c on cardiac development and its possible mechanism in&amp;nbsp;vivo. Zebrafish embryos were microinjected with different doses (1, 1.6 and 2&amp;nbsp;&amp;micro;mol) miR-29c mimics or negative controls, and hatchability, mortality and cardiac malformation were subsequently observed. The results showed that in zebrafish embryos, miR-29c overexpression attenuated heart development in a dose-dependent manner, manifested by heart rate slowdown, pericardial edema and heart looping disorder. Further experiments showed that overexpression of miR-29c was associated with the Wnt4/&amp;beta;-catenin signaling pathway to regulate zebrafish embryonic heart development. In conclusion, the present results demonstrated that miR-29c regulated the lateral development and cardiac circulation of zebrafish embryo by targeting Wnt4.

MicroRNA-29c affects zebrafish cardiac development via targeting Wnt4