[Cardiomycyte overexpression of miR-27b resulted in cardiac fibrosis and mitochondria injury in mice].

Previous microRNA(miRNA) array results have shown that the expression of miR-27b is upregulated in heart tissues from human cardiomyopathy and pressure-overloaded hypertrophic mouse model,implying that miR-27b might play an 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 matrix metalloproteinase 13(MMP13),a key regulator involved in cardiac fibrosis,was the target of miR-27b.The expression of MMP13 was decreased and the expression of Col I and III was increased in miR-27b transgenic mice..In addition,defects in ultrastructral architecture were also found in miR-27b transgenic mice.The above results demonstrated that miR-27b might promote cardiac fibrosis through inhibiting MMP13.