Biotechnology Letters

, Volume 38, Issue 4, pp 579–587

Restoration of miR-98 relieves the inhibitory effect of nicotine on the differentiation of P19 cells into cardiomyocytes

Original Research Paper

DOI: 10.1007/s10529-015-2030-y

Cite this article as:
Ai, F., Zhang, Y. & Peng, B. Biotechnol Lett (2016) 38: 579. doi:10.1007/s10529-015-2030-y
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Abstract

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.

Keywords

Cardiomyocytes Congenital heart defect miR-98 Myocardial differentiation Nicotine P19 cells Wnt1 

Copyright information

© Springer Science+Business Media Dordrecht 2015

Authors and Affiliations

  1. 1.Department of Cardiovascular SurgeryHenan Provincial People’s Hospital, People’s Hospital of Zhengzhou UniversityZhengzhouPeople’s Republic of China

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