Adult-ATF3 expressing mice display higher fibrosis and lower heart function following a 2-week pressure overload model.

Abstract

<p>RT-qPCR analysis for cDNA derived from either wild-type or ATF3 transgenic mice. mRNA was extracted from ventricles from wild-type (black) or ATF3 transgenic (gray) and RT-qPCR was performed with the indicated specific primers: <b>A</b>. Col1α <b>B</b>. TGFβ <b>C</b>. connective tissue growth factor (cTGF). The results represent the mean and SEM relative to GAPDH expression of the indicated number of animals (n). <b>D</b>. Masson trichrome staining of paraffin embedded sections of wild-type and adult-ATF3 expressing mice, either untreated (control) or after 2 weeks of PE infusion. <b>E</b>. Quantification of fibrosis of the indicated number of mice (n). At least five sections for the indicated number of mice (n) were analyzed <b>F</b>. Adult-ATF3 expressing mice treated as indicated were examined by micro-ultrasound and measurements were recorded to determine fractional shortening (FS) percentage in order to assess heart function. Maximal left ventricles end-diastolic (LVDd) and end-systolic (LVDs) dimensions parameters were measured in short-axis M-mode images. Fractional shortening (FS) was calculated as: FS (%) = [(LVDd-LVDs)/LVDd] X 100. The results represent the mean and SEM of the indicated number of animals (n). Asterisks (*/**) indicate a P value <0.05 or <0.01 respectively of a one-tailed t-test compared to wild-type mice.</p

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