Cardiac miRNA profiling during pressure overload-induced hypertrophy in PTP1B-deficient mice

The switch from the faster α-MHC to the slower β-MHC isoform that occurs in cardiac hypertrophy is generally thought to reduce contractile performance and to contribute to functional maladaptation. This MHC switch is regulated by miRNAs and thyroid hormones in development and hypertrophy. Since exacerbated hypertrophy is observed in absence of β-MHC expression in PTP1B cKO mice, we speculated that PTP1B inactivation associated with pressure-overload hypertrophy could disrupt miRNAs homeostasis. In this dataset, expression status of 1908 mouse miRNAs was investigated and reveal that PTP1B contribute to gene silencing by mediating miRNA loading onto the RISC complex. Cardiac miRNA populations were extracted from sham and TAC PTP1B floxed and PTP1B cKO mice 4 weeks post-surgery. The RNAs were then analyzed on an Affimetrix 4.0 miRNA Array. Intensity values were transformed into log2 scale, and the heat map shows log2 fold change values for each data set