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Physiol. Genomics 27: 309-317, 2006. First published August 1, 2006; doi:10.1152/physiolgenomics.00072.2006
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Microarray analysis of gene expression during early stages of mild and severe cardiac hypertrophy

¹ Department of Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati College of Medicine, Cincinnati, Ohio
² Division of Biomedical Informatics, Children's Hospital Medical Center, Cincinnati, Ohio
³ Institute of Molecular Pharmacology and Biophysics, Department of Surgery, University of Cincinnati College of Medicine, Cincinnati, Ohio

Familial hypertrophic cardiomyopathy (FHC) is a disease characterized by ventricular hypertrophy, fibrosis, and aberrant systolic and/or diastolic function. We previously developed two transgenic mouse models that carry FHC-associated mutations in -tropomyosin (TM): FHC -TM175 mice show patchy areas of mild ventricular disorganization and limited hypertrophy, whereas FHC -TM180 mice exhibit severe hypertrophy and fibrosis and die within 6 mo. To obtain a better understanding of the molecular mechanisms associated with the early onset of cardiac hypertrophy, we conducted a detailed comparative analysis of gene expression in 2.5-mo-old control, FHC -TM175, and -TM180 ventricular tissue. Results show that 754 genes (from a total of 22,600) were differentially expressed between the nontransgenic (NTG) and the FHC hearts. There are 178 differentially regulated genes between NTG and the FHC -TM175 hearts, 388 genes are differentially expressed between NTG and FHC -TM180 hearts, and 266 genes are differentially expressed between FHC -TM175 and FHC -TM180 hearts. Genes that exhibit the largest increase in expression belong to the "secreted/extracellular matrix" category, and those with the most significant decrease in expression are associated with "metabolic enzymes." Confirmation of the microarray analysis was conducted by quantitative real-time PCR on gene transcripts commonly associated with cardiac hypertrophy.

tropomyosin; cardiomyopathy; familial hypertrophic cardiomyopathy mutations; microarray