microRNA expression data from a heterozygous Titin-deficient mouse model and wildtype controls

Mutations in the sarcomeric protein titin are a major cause of human dilated cardiomyopathy. We have developed a knock-in mouse model that imitated a previously identified titin truncation mutation. The heterotygous Ttn-deficient mice develop features of DCM and therefore recapitulate the human phenotype. To investigate the role of microRNAs in titin-based heart failure, we performed a miRNA screen in heterozygous Ttn-deficient mice and their wildtype littermate controls. Heterozygous Ttn knock-in mice and theit wildtype littermate controls were challenged with Angiotensin II infusion for 3 days. RNA was extracted and hybridized to Affymetrix microRNA microarrays.