Fig. 2 | Signal Transduction and Targeted Therapy

Fig. 2

From: The double face of miR-320: cardiomyocytes-derived miR-320 deteriorated while fibroblasts-derived miR-320 protected against heart failure induced by transverse aortic constriction

Fig. 2

MiR-320 expression patterns were opposite between isolated CMs and CFs from TAC mice. a C57BL/6 mice were killed to either sham operation (n = 16) or TAC and noted after 3, 7, 14, 28, or 70 days (n = 15, 15, 17, 14, or 13, respectively). Representative short axis images of echocardiograms. b Gross morphologies of hearts from mice after TAC at different time points are shown. c The ratios of heart weight and body weight in mice after TAC. d, e LVEF% and LVFS% were detected by echocardiography. f, g Hemodynamic parameters of mice with different treatments were measured by the Millar cardiac catheter system. dp/dtmax, peak instantaneous rate of LV pressure increase; dp/dtmin, peak instantaneous rate of LV pressure decrease. h, i ANP and β-MHC mRNA levels in the hearts were detected by real-time PCR. j MiR-320 expression levels in the hearts were quantified by real-time PCR. k The expressions of miR-320 in isolated CMs were measured by real-time PCR. l Real-time PCR analysis of miR-320 in isolated CFs. ANP Atrial natriuretic peptide, β-MHC β-myosin heavy chain, LVEF left ventricular ejection fraction, LVFS left ventricular fractional shortening; Data are presented as mean ± SEM

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