Abstract
The placenta regulates nutrient transport and plays a central role in fetal growth. Disturbances in placental function during critical periods of development set the stage for fetal programming of adult diseases. DNA methylation of placental genes may be one of the mechanisms by which placental function is altered and fetal adaptations leading to developmental programming occur. Our goal was to evaluate the global DNA methylation status in a previously characterized transgenic mouse model of utero-placental insufficiency and fetal vascular programming.
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