We have demonstrated that changes in cardiomyocyte viability, lack of adaptive capillary growth, fibrosis, and response to metabolic stress are differentially regulated in LV-AOB and RV-PAB ( 11, 13, 16, 20).

Our previous studies using the rabbit model of LV-AOB and RV-PAB have demonstrated that disease progression involves both cellular and extracellular components of the myocardium. These changes allow for maintenance of contractile function in left ventricular pressure-overload hypertrophy, whereas in right ventricular pressure-overload hypertrophy these changes are less effective and progression to failure occurs more rapidly ( 2, 4, 15). Initially, the myocardium compensates to elevated pressure-loading by increasing wall thickness to normalize wall stress. Ventricular outflow tract obstruction in congenital heart defects such as interrupted aortic arch, coarctation of the aorta on the left side, and pulmonary artery stenosis on the right side, causes progressive cardiac hypertrophy and, if unrelieved, leads to ventricular dilatation with contractile dysfunction and ultimately irreversible heart failure. The identification of these pathways should allow for the development of specific therapeutic interventions for targeted treatment and amelioration of LV-AOB and RV-PAB to ameliorate morbidity and mortality. These results identify divergent transcript and protein expression profiles in LV-AOB and RV-PAB and provide new insight into the biological basis of ventricular specific hypertrophy.

In RV-PAB there is also an increased transcript expression levels for cardiac oxidative phosphorylation but increased protein expression levels for structural constituents of muscle, cardiac muscle tissue development, and calcium handling. Microarray and proteomic data demonstrate that in LV-AOB there is increased transcript expression levels for oxidative phosphorylation, mitochondria energy pathways, actin, ILK, hypoxia, calcium, and protein kinase-A signaling and increased protein expression levels of proteins for cellular macromolecular complex assembly and oxidative phosphorylation. After 4 (LV-AOB) and 6 (RV-PAB) wk recovery, the hearts were removed and matched RNA and proteins samples were isolated for microarray and proteomic analysis. Controls ( n = 6 each) were sham-manipulated. RV-PAB was achieved by banding the pulmonary artery ( n = 6). Newborn New Zealand White rabbits underwent banding of the descending thoracic aorta. In this report we use microarray and proteomic analyses to identify pathways modulated by LV-aortic banding (AOB) and RV-pulmonary artery banding (PAB) in the immature heart. Right ventricular (RV) and left ventricular (LV) myocardium differ in their pathophysiological response to pressure-overload hypertrophy.

Raw data aob extractor