Cardiac overexpression of miR-130a results in decreased FOG-2 expression and a thin ventricular myocardial wall.

<p>In (A), expression of miR-130a as determined by quantitative RT-PCR on four wild type (WT) and four transgenic hearts (TG-1 thru 4) at embryonic day 13.5. Results represent the mean±S.E.M. of three separate experiments performed in duplicate. ‘*’ indicates statistically significant difference from wild-type, p<0.002. In (B), western analysis of wild type (WT) and transgenic hearts (TG-5 thru 8) using an anti-FOG-2 antibody. Western analysis of Lamin B was used as a control for equal protein loading. Quantitation of this blot is shown in (C), with wild type levels of FOG-2 set to 100%. In (D - G), transverse sections of embryonic day 14.5 hearts from wild type (D, F) and β-MHC-miR-130a transgenics (E, G) stained with hematoxylin and eosin. Note the ventricular septal defect (arrow, E) and the thin compact zone of ventricular myocardium (arrowheads, F compared to G) seen in the transgenic embryos. In (H), echocardiographic determination of left ventricular fractional shortening (left panel) and left ventricular end diastolic diameter (right panel) in embryonic day 14.5 transgenic and non-transgenic embryos. ‘*’ indicates a statistically significant difference (p<0.0005).