Abstract: Previous microRNA array results have shown that miR-27b is upregulated in heart tissue from human cardiomyopathy and pressure-overloaded hypertrophic mouse model, implying that miR-27b might play important role in heart diseases. To study the in vivo function of miR-27b, we generated a transgenic mouse line overexpressing miR-27b under the control of the 5.5 kb promoter of ?-myosin heavy chain (?-MHC). Real-time PCR results demonstrated that miR-27b precursor and mature miR-27b were significantly increased in the heart tissues of miR-27b transgenic mice. miR-27b transgenic mice not only displayed cardiac hypertrophy, but also exhibited significant cardiac fibrosis. Further study showed that MMP13, a key regulator involved in cardiac fibrosis, was the target of miR-27b, and miR-27b transgenic mice displayed decreased expression of MMP13 and increased expression of Col I and III. In addition, defects in ultrastructral architecture were also found in miR-27b transgenic mice. The above results demonstrated that miR-27b might inhibit MMP13 to promote cardiac fibrosis.

Key words: miR-27b, cardiomyocyte, transgenic mice, cardiac fibrosis, MMP13