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Clinical and Translational Medicine
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Open Access 01-12-2017 | Short report

Deletion of Cdc42 in embryonic cardiomyocytes results in right ventricle hypoplasia

Authors: Yang Liu, Jian Wang, Jieli Li, Rui Wang, Binu Tharakan, Shenyuan L. Zhang, Carl W. Tong, Xu Peng

Published in: Clinical and Translational Medicine | Issue 1/2017

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Abstract

Background

Cdc42 is a member of the Rho GTPase family and functions as a molecular switch in regulating cytoskeleton remodeling and cell polarity establishment. Inactivating Cdc42 in cardiomyocytes resulted in embryonic lethality with heart developmental defects, including ventricular septum defects and thin ventricle wall syndrome.

Findings

In this study, we have generated a Cdc42 cardiomyocyte knockout mouse line by crossing Cdc42/flox mice with myosin light chain 2a (MLC2a)-Cre mice. We found that the deletion of Cdc42 in embryonic cardiomyocytes resulted in an underdeveloped right ventricle. Microarray analysis and real-time PCR data analysis displayed that the deletion of Cdc42 decreased dHand expression level. In addition, we found evaginations in the ventricle walls of Cdc42 knockout hearts.

Conclusion

We concluded that Cdc42 plays an essential role in right ventricle growth.
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Metadata
Title
Deletion of Cdc42 in embryonic cardiomyocytes results in right ventricle hypoplasia
Authors
Yang Liu
Jian Wang
Jieli Li
Rui Wang
Binu Tharakan
Shenyuan L. Zhang
Carl W. Tong
Xu Peng
Publication date
01-12-2017
Publisher
Springer Berlin Heidelberg
Published in
Clinical and Translational Medicine / Issue 1/2017
Electronic ISSN: 2001-1326
DOI
https://doi.org/10.1186/s40169-017-0171-4

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