Jian Wang et al. npg 521 (LV) enlargement (Figure 4A and 4B), and showed that the cardiomyocytes of the transgenic mice were larger than those of the control mice using laminin immunohis- tochemistry (Figure 4C and 4D). Quantitative measure- ment of miR-27b transgenic cardiomyocytes revealed a 32% increase in cell cross-sectional area relative to controls (Figure 4G). We also measured the cell size of the individual cardiomyocytes in isolated adult myocyte preparations (Figure 4E and 4F). The mean cell area of the cardiomyocytes (n = 150) obtained from three-month- old miR-27b transgenic mice (n = 4) was greater than that of those obtained from the control mice (Figure 4H). These observations indicated that miR-27b overex- pression in vivo is sufficient to induce cardiac hypertro- phy, which may be largely due to the increased size of cardiomyocyte. miR-27b transgenic mice developed impaired cardiac function To evaluate the effect of miR-27b overexpression on cardiac function, we first assessed the LV dimensions and the systolic functions of 3-month-old and 6-month- Figure 5 Cardiac dysfunction in miR-27b transgenic mice. (A) Representative M-mode images of miR-27b Tg mice (right) and littermate controls (left). (B, C) Measurements of the LV wall thickness in systole (LVPWs) and diastole (LVPWd). (D, E) Measurements of the LV internal diameters in systole (LVIDs) and diastole (LVIDd). (F-H) Quantification of ratio of LV mass to body weight (LVM/BW), ejection fraction (EF) and fractional shortening (FS). Mean values ± SEM were determined by echocardiography. (I, J) Quantification of the LV diastolic end pressure (LVEDP), the mean arterial blood pressure (MAP) in hearts from miR-27b Tg mice and control mice at the age of 3 and 6 months. Mean values ± SEM were determined by hemo- dynamic analysis. *P < 0.05, significantly different from age-matched controls. www.cell-research.com | Cell Research