Inflammation‐induced left ventricular fibrosis is partially mediated by tumor necrosis factor‐α

Figures

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  FIGURE 1. LV geometry and extracellular matrix gene expression. Relative mRNA expression of TGFβ (a), Col1 (b), LOX (c), α‐SMA (d), echocardiographic measurement of relative wall thickness (RWT) of the left ventricles (e). Group differences are determined by two‐way analysis of variance (ANOVA) with group and sex as the main effects, followed by Tukey's post hoc tests. In (a)–(d), results are expressed in arbitrary units normalized for the expression of the endogenous reference gene, HPRT. Data are presented as means ± SEM (a‐e); * p < 0.05 versus control; ** p < 0.01 versus control; ***p < 0.001 versus control; ****p < 0.0001 versus control; † p < 0.05 versus CIA. Contribution of Col1, LOX, TGFβ, CD68, α‐SMA, and Myh7 in left ventricular tissues to relative wall thickness is (f) determined by linear regression. Open circles represent standardized beta coefficients and error bars represent 95% CI

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  FIGURE 2. LOX and COL1 markers of ECM gene expression. Pearson's correlations of TGFβ and CD68 with Col1 and LOX in all groups (a, b) and control versus CIA groups only (c, d). Open circles represent correlation coefficients and error bars represent 95% CI

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  FIGURE 3. Expression of matrix metalloproteinases and measures of diastolic dysfunction. Relative mRNA expression of MMP2 (a) and MMP9 (b) in left ventricular tissues and echocardiographic measures, e’ (c) and e’/a’ (d) of control, CIA, and anti‐TNF‐α rats. Group differences are determined by two‐way analysis of variance (ANOVA) with group and sex as the main effects, followed by Tukey's post hoc tests. mRNA expression data expressed in arbitrary units normalized for the expression of the endogenous reference gene, HPRT1. Data are presented as means ± SEM; *p < 0.05 versus control; **p < 0.01 versus control; ***p < 0.001 versus control; ****p < 0.0001 versus control; †††† p < 0.0001 versus anti‐TNF‐α