Open AccessDeletion of Cdc42 in embryonic cardiomyocytes results in right ventricle hypoplasia
Author(s) -
Liu Yang,
Wang Jian,
Li Jieli,
Wang Rui,
Tharakan Binu,
Zhang Shenyuan L.,
Tong Carl W.,
Peng Xu
Publication year - 2017
Publication title -
clinical and translational medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.125
H-Index - 1
ISSN - 2001-1326
DOI - 10.1186/s40169-017-0171-4
Subject(s) - ventricle , cdc42 , embryonic stem cell , microbiology and biotechnology , knockout mouse , medicine , biology , actin , genetics , gene , receptor
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.