Deletion of Cdc42 in embryonic cardiomyocytes results in right ventricle hypoplasia

Clinical and Translational Medicine - Tập 6 Số 1 - 2017
Yang Liu1,2, Jian Wang1, Jieli Li1, Rui Wang1,3, Binu Tharakan4, Shenyuan L. Zhang1, Carl W. Tong1,5, Peng Xu1
1Department of Medical Physiology College of Medicine Texas A&M University Temple USA
2Department of Obstetrics and Gynecology Baylor Scott & White Health Temple USA
3Yangpu District Central Hospital Tongji University Shanghai China
4Department of Surgery Baylor Scott & White Health Temple USA
5Internal Medicine/Cardiology Division Baylor Scott & White Health Temple USA

Tóm tắt

AbstractBackgroundCdc42 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.FindingsIn 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.ConclusionWe concluded that Cdc42 plays an essential role in right ventricle growth.

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Clinical and Translational Medicine

Tập 6 Số 1

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