Conclusions
Restoration of miR-98 relieves the inhibitory effect of nicotine on differentiation of P19 cells via targeting the 3'-UTR of Wnt1, which offers novel insights into our understanding of underlying molecular mechanisms of congenital heart defects.
Objective
To study whether miR-98 participates in the effects of nicotine on myocardial differentiation.
Results
By western blot, MTT and flow cytometry assays, we found that nicotine suppresses P19 cell differentiation into cardiomyocytes and apoptosis, and promotes proliferation, while restoration of miR-98 relieves the inhibitory effect of nicotine on the P19 cell differentiation. By target prediction analysis and luciferase reporter assay, we observed that miR-98 inhibits the protein expression of Wnt1 by directly acting on the 3'-UTR of Wnt1 mRNA. We assumed that the effect of miR-98 on Wnt1 might alter the activity of the Wnt1/β-catenin signaling pathway and be associated with myocardial differentiation. In summary, nicotine restrains differentiation of P19 cells into cardiomyocytes and decreases the level of miR-98. Conclusions: Restoration of miR-98 relieves the inhibitory effect of nicotine on differentiation of P19 cells via targeting the 3'-UTR of Wnt1, which offers novel insights into our understanding of underlying molecular mechanisms of congenital heart defects.