Gene expression levels of the IFN regulatory factors <i>Irf3</i> and <i>Irf7</i> in different HF models of diverse etiology.

<p>Cardiac tissue of healthy and diseased C57BL/6J mice was used for TaqMan based gene expression analysis of the IFN regulatory factors <i>Irf3</i> and <i>Irf7</i>. Expression levels of cardiac tissue from control mice are shown as white boxes, from diseased animals as red, blue, green or yellow boxes corresponding to the analyzed heart failure model. In viral-induced myocarditis (shown in red), gene expression of <i>Irf7</i> showed by far the highest increase 7 days after infection compared to healthy controls. However, <i>Irf3</i> displayed no changes in gene expression during viral myocarditis. Moreover, in the model of myocardial infarction (shown in blue), gene expression of <i>Irf3</i> and <i>Irf7</i> was highly increased 5 days post infarction in the scar tissue when compared to the non-infarcted LV or sham, whereas <i>Irf7</i> showed a clearly higher gene expression when compared to the expression of <i>Irf3</i>. In STZ-induced diabetic cardiomyopathy (shown in green), an opposite effect on gene expression of <i>Irf3</i> and <i>Irf7</i> was observed. Whereas, <i>Irf3</i> showed a decreased gene expression, <i>Irf7</i> displayed an increased gene expression under diabetic conditions. However, in the heart failure model caused by chronic AngII-infusion for 21 days (shown in yellow), no differences in gene expression of <i>Irf3</i> and <i>Irf7</i> were detected. Data are presented in box plots as relative mRNA expression in fold change to the corresponding untreated control using the formula 2^−ΔΔCt. * = significantly different compared to corresponding control; ^# = significantly different compared to VM (acute—7 days) or RZ (remote zone).