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1 Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati College of Medicine, Cincinnati, Ohio, United States
2 Division of Biomedical Informatics, Children's Hospital Medical Center, Cincinnati, Ohio, United States
3 Institute of Molecular Pharmacology and Biophysics, University of Cincinnati, Cincinnati, Ohio, United States
4 Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati College of Medicine, Cincinnati, Ohio, United States
* To whom correspondence should be addressed. E-mail: david.wieczorek{at}uc.edu.
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 months. 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-month-old control, FHC -TM175, and -TM180 ventricular tissue. Results show that 754 genes (from a total of 22,600) were differentially expressed between the 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.
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