Gene expression profiling in cardiac AngII-overexpressing mice (TG1306/1R)

Agonist-induced cardiac hypertrophy in TG1306/1R transgenic mice with cardiac angiotensin II overproduction leads to a gradual transition from a compensatory hypertrophic state to heart failure. To gain insight into the molecular mechanisms that play a role in maintaining cardiac integrity in the diseased heart, we performed a comparative study of gene expression between wild-type (WT) and transgenic (TG) hearts using microarray analysis. TG1306/1R transgenics were separated into two phenotypic groups (hypertrophic and dilated) based on morphological parameters (cardiac weight index and histology) and either a moderate (hypertrophic) or a high (dilated) upregulation of molecular markers for hypertrophy and failure, and compared to age and sex-matched wild-types. In this series, twelve 60 week old male TG1306/1R mice were separated into 3 groups: WT1-4= Four Wild-types TG1306/1R littermates genetically negative for the transgene (-/-) Hyp1-4= Four TG1306/1R mice heterozygote for the transgene (-/+) and developing a concentric hypertrophic phenotype* Dil1-4 = Four TG1306/1R mice heterozygote for the transgene (-/+) and developing a dilated cardiac phenotype* This series contains 4 biological replicates for the following triangulation: WT is compared to Hyp, WT is compared to Dil, and Hyp is compared to Dil. * For further information read: Domenighetti AA, Wang Q, Egger M, Richards SM, Pedrazzini T, Delbridge LM. Angiotensin II-mediated phenotypic cardiomyocyte remodeling leads to age-dependent cardiac dysfunction and failure. Hypertension. 2005 Aug;46(2):426-32. [PMID: 15998712]