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Fig. 2 | Journal of Translational Medicine

Fig. 2

From: The redox-active defensive Selenoprotein T as a novel stress sensor protein playing a key role in the pathophysiology of heart failure

Fig. 2

Effect of PSELT on cardiac ultrastructure and on protein expression of SELENOT and fibrosis/senescence-related markers in cardiac tissues. A Ultrastructure representations obtained by transmission electron microscopy (TEM) on cardiac sections of control animals (WST) and SHHF animals chronically treated with or without PSELT (scale bar: 2 μm). B Western blot analysis of desmin in soluble and insoluble fractions of WST, WST + PSELT, SHHF, SHHF + PSELT hearts. C Gelatin SDS-PAGE zymographic analysis of MMP-2 activity in myocardial tissues. Western blot analysis of CTGF, p53, p21, γH2AX, SELENOT, in the hearts of WST, WST + PSELT, SHHF, SHHF + PSELT groups (n = 3). Histograms represent the ratio of densitometric analysis of protein:loading control. Data are expressed as the mean ± SEM (n = 3 independent experiments). Significant differences were detected by one-way ANOVA and Newman-Keuls multiple comparison test. *p < 0.05; **p < 0.01, ***p < 0.001

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