Extensive induction of important mediators of fibrosis and dystrophic calcification in desmin-deficient cardiomyopathy.

ABSTRACT: Mice lacking the intermediate filament protein desmin demonstrate abnormal mitochondria behavior, disruption of muscle architecture, and myocardial degeneration with extensive calcium deposits and fibrosis. These abnormalities are associated with cardiomyocyte hypertrophy, cardiac chamber dilation and eventually with heart failure. In an effort to elucidate the molecular mechanisms leading to the observed pathogenesis, we have analyzed gene expression changes in cardiac tissue using differential display polymerase chain reaction and cDNA atlas array methods. The most substantial changes were found in genes coding the small extracellular matrix proteins osteopontin and decorin that are dramatically induced in the desmin-null myocardium. We further analyzed their expression pattern both at t

SUBMITTER: Mavroidis M 

PROVIDER: S-EPMC1867168 | biostudies-literature | 2002 Mar

REPOSITORIES: biostudies-literature