Deletion of Cdc42 in embryonic cardiomyocytes results in right ventricle hypoplasia

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 defect...

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Detalles Bibliográficos
Autores principales: Liu, Yang, Wang, Jian, Li, Jieli, Wang, Rui, Tharakan, Binu, Zhang, Shenyuan L., Tong, Carl W., Peng, Xu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2017
Materias:
Short Report
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5670094/
https://www.ncbi.nlm.nih.gov/pubmed/29101495
http://dx.doi.org/10.1186/s40169-017-0171-4
Descripción
Sumario: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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