premier biosoft beacon designer 8.02 versions

However, galectin-3 loss did not affect survival, systolic and diastolic dysfunction, cardiac fibrosis, and cardiomyocyte hypertrophy in the pressure-overloaded heart. Real-time PCR primers were designed using Beacon Designer (v 8.02, Premier Biosoft, California) and the validation proceeded using the target primers and the internal reference transcript, RPL10, primers listed in Table 1.

Galectin-3 knockout mice exhibited accelerated cardiac hypertrophy after 7 days of pressure overload, whereas female galectin-3 knockouts had delayed dilation after 28 days of transverse aortic constriction. The Trinity assembly pipeline, release version, was used for de novo assembly of the trimmed RNAseq reads (Grabherr et al. Correlation studies revealed that cardiomyocyte- but not macrophage-specific galectin-3 localization was associated with adverse remodeling and dysfunction. In vitro, cytokine stimulation suppressed galectin-3 synthesis by macrophages and cardiac fibroblasts. Early up-regulation of galectin-3 was localized in subpopulations of macrophages and myofibroblasts however, after 7 to 28 days of transverse aortic constriction, a subset of cardiomyocytes in fibrotic areas contained large amounts of galectin-3. In a mouse model of transverse aortic constriction, galectin-3 expression was markedly up-regulated in the pressure-overloaded myocardium. In normal mouse myocardium, galectin-3 was constitutively expressed in macrophages and was localized in atrial but not ventricular cardiomyocytes. We hypothesized that galectin-3 may be up-regulated in the pressure-overloaded myocardium and regulate hypertrophy and fibrosis. Galectin-3 regulates inflammatory and fibrotic responses however, its role in cardiac remodeling remains unclear. The β-galactoside–binding animal lectin galectin-3 is predominantly expressed by activated macrophages and is a promising biomarker for patients with heart failure.

Premier biosoft beacon designer 8.02 versions