Microarray analysis reveals pivotal divergent mRNA expression profiles early in the development of either compensated ventricular hypertrophy or heart failure.

摘要: Myocardial right ventricular (RV) hypertrophy due to pulmonary hypertension is aimed at normalizing wall stress. Depending on the degree of pressure overload, RV may progress a state impaired contractile function and heart failure, but this cannot be discerned during early stages remodeling. We tested whether critical differences in gene expression profiles exist between ventricles before ultimate development either compensated or decompensated hypertrophic phenotype. Both phenotypes were selectively induced Wistar rats by single subcutaneous injection low high dose pyrrolizidine alkaloid monocrotaline (MCT). Spotted oligonucleotide microarrays used investigate pressure-dependent cardiac 2 wk after MCT injections, control that would ultimately develop hypertrophy. Clustering significantly regulated genes revealed specific for each group, although was still similar both. The destined failure showed activation pro-apoptotic pathways, particularly related mitochondria, whereas group developing blocked pro-death effector signaling via p38-MAPK, through upregulation MAPK phosphatase-1. In summary, we show that, already an time point, pivotal will phenotype, depending overload. These data reveal provide markers prediction clinical outcome as well potential targets intervention.