Altering Bmp4 expression in the mouse myocardium recapitulates the range of atrioventricular canal defects seen in patients, identifying Bmp4 as a direct mediator of atrioventricular septation.
Does altering Bmp4 expression in the myocardium cause atrioventricular septation defects in a mouse model?
This study establishes Bmp4 as an essential myocardial signal for atrioventricular septation and provides a genetic mouse model for atrioventricular canal defects.
Proper septation and valvulogenesis during cardiogenesis depend on interactions between the myocardium and the endocardium. By combining use of a hypomorphic Bone morphogenetic protein 4 (Bmp4) allele with conditional gene inactivation, we here identify Bmp4 as a signal from the myocardium directly mediating atrioventricular septation. Defects in this process cause one of the most common human congenital heart abnormalities, atrioventricular canal defect (AVCD). The spectrum of defects obtained through altering Bmp4 expression in the myocardium recapitulates the range of AVCDs diagnosed in patients, thus providing a useful genetic model with AVCD as the primary defect.
Jiao et al. (Wed,) conducted a other in Atrioventricular canal defect (AVCD). Bmp4 gene inactivation was evaluated on Atrioventricular septation. Altering Bmp4 expression in the mouse myocardium recapitulates the range of atrioventricular canal defects seen in patients, identifying Bmp4 as a direct mediator of atrioventricular septation.
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