MicroRNA-150 Protects Against Pressure Overload-Induced Cardiac Hypertrophy

Cardiac hypertrophy is the response of the heart to a variety of hypertrophic stimuli; this condition progresses to heart failure and sudden death. MicroRNAs (miRs) are a family of small, non-coding RNAs that mediate posttranscriptional gene silencing. Recent studies have identified miRs as important regulators in cardiac hypertrophy. One specific miR, miR-150 has been reported to be downregulated in hypertrophic murine hearts. However, the role of miR-150 as a regulator of cardiac hypertrophy remains unclear. In the present study, we used gain-of-function and loss-of-function approaches to investigate the functional roles of miR-150 in cardiac hypertrophy induced by aortic banding. The extent of the cardiac hypertrophy was evaluated by echocardiography and by pathological and molecular analyses of heart samples. Our results revealed that transgenic mice that overexpress miR-150 in the heart were resistant to cardiac hypertrophy and fibrosis through down-regulation of serum response factor (SRF). Conversely, the loss of function of miR-150 by genetic knockdown or antagomiR approaches produced the opposite effects. These studies suggest that miR-150 plays an important role in the regulation of cardiac hypertrophy and SRF is involved in miR-150 mediated anti-hypertrophic effect. Thus, miR-150 may be a new therapeutic target for cardiac hypertrophy.