Targeted Inactivation of Cerberus Like-2 Leads to Left Ventricular Cardiac Hyperplasia and Systolic Dysfunction in the Mouse

Araújo, Ana Carolina; Marques, Sara; Belo, José A.

http://hdl.handle.net/10400.1/11366

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Authors

Araújo, Ana Carolina

Marques, Sara

Belo, José A.

Abstract(s)

Previous analysis of the Cerberus like 2 knockout (Cerl2(-/-)) mouse revealed a significant mortality during the first day after birth, mostly due to cardiac defects apparently associated with randomization of the left-right axis. We have however, identified Cerl2-associated cardiac defects, particularly a large increase in the left ventricular myocardial wall in neonates that cannot be explained by laterality abnormalities. Therefore, in order to access the endogenous role of Cerl2 in cardiogenesis, we analyzed the embryonic and neonatal hearts of Cerl2 null mutants that did not display a laterality phenotype. Neonatal mutants obtained from the compound mouse line Cer2(-/-)

Keywords

Congenital heart-disease Cell-cycle regulation Embryonic stem-cells Echocardiographic-assessment Transcription factors Gene-expression Arterial pole Chick-embryo Field Cardiomyogenesis