Transcription profiling of mice hearts comparing microRNA-22 overexpression to wildtype

To explore the role of miR-22 in the heart, we generated miR-22 null and transgenic mice. Cardiac transgenic overexpression of miR-22 in vivo led to cardiac hypertrophy that evolved into progressive dilated cardiomyopathy (DCM) in unstressed hearts. We found that miR-22 directly regulates two transcriptional antagonists, purine rich element binding protein B (PURB), a repressor, and serum response factor (SRF), an activator, in the heart. Through these gain- and loss-of-function experiments in mice, we suggest that a primary function of miR-22 is to fine tune the relative expression and activity of these two transcriptional antagonists to influence contractile gene expression, function, growth and adaptation of the heart to stress.