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Maternal loss of imprinting (LOI) at the  H19/IGF2  locus results in biallelic  IGF2  and reduced  H19  expression and is associated with Beckwith–-Wiedemann syndrome (BWS). We use mouse models for LOI to understand the relative importance of  Igf2  and  H19  mis-expression in BWS phenotypes. Here we focus on cardiovascular phenotypes and show that neonatal cardiomegaly is exclusively dependent on increased  Igf2 . Circulating IGF2 binds cardiomyocyte receptors to hyperactivate mTOR signaling, resulting in cellular hyperplasia and hypertrophy. These  Igf2 -dependent phenotypes are transient: cardiac size returns to normal once  Igf2  expression is suppressed postnatally. However, reduced  H19  expression is sufficient to cause progressive heart pathologies including fibrosis and reduced ventricular function. In the heart,  H19  expression is primarily in endothelial cells (ECs) and regulates EC differentiation both in vivo and in vitro. Finally, we establish novel mouse models to show that cardiac phenotypes depend on  H19  lncRNA interactions with  Mirlet7  microRNAs.

Cardiac pathologies in mouse loss of imprinting models are due to misexpression of H19 long noncoding RNA