Anne-Marie Koop

264 control hearts upon RV pressure overload, Rcan1.4 mRNA levels were significantly decreased in the knockout LVs, under similar conditions, compared to the control LVs ( figure 3h ). Although increased collagen deposition and fibrotic lesions were observed in the LVs of the control mice subjected to PAB, this was not observed in knockout animals ( figure 3i ). Similar results were obtained regarding mRNA levels for Col1A , Tgf β and Eng in the LV tissue ( figure 3j-l ). When assessing the capillary density of the LV in our different experimental groups we observed higher capillary density in the control mice compared to the knockout animals, in both sham and PAB groups, despite a decrease in the overloaded groups ( figure 3m ). The lower capillary density observed at baseline in the Hand2 knockout animals was evenmore reduced upon RVstress ( figure 3m ). This was in line with the expression profile of Vegfr2 , which although not significant did show a trend to decrease in the absence of Hand2, either at baseline or under RV stress conditions ( figure 3n ). These data suggest that RV pressure overload results in deformation of the LV with preserved LV function. Furthermore, while silencing of Hand2 seems to ameliorate the molecular maladaptive response of the LV to RV stress, vascular remodelling remains slightly impaired. Silencing of Hand2 seems to ameliorate the molecular maladaptive response of the left ventricle to right ventricular stress.