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. 2012 Mar;180(3):929–939. doi: 10.1016/j.ajpath.2011.11.007

Figure 5.

Figure 5

Features of cardiac hypertrophy and fibrosis are observed in Nfkb1 knockout mice. A: Heart sections were stained for α-sarcomeric actin and sarcomeric units were counted. The mean number (Ave) of sarcomeric units in Nfkb1−/− mice was significantly increased, compared with WT. *P = <0.05. B: Representative photomicrographs of laminin-stained WT and Nfkb1−/− mouse hearts. Mean cardiomyocyte cytoplasmic/nuclear area ratios were calculated using image analysis software. The ratio was significantly increased in Nfkb1−/− hearts, compared with WT. **P < 0.01. C: Representative photomicrographs of Sirius Red-stained heart sections from WT and Nfkb1−/− mice. Densitometric analysis revealed a statistically significant increase in collagen deposition (red fibers) in Nfkb1−/− mice. *P = <0.05. Data are expressed as means ± SEM of eight WT and six Nfkb1−/− mice. +ve, positive. D: Relative mRNA levels of the transcriptional regulators of hypertrophy myocyte enhancer factor 2 (Mef2) A, C, and D (but not Mef2B), Gata4, and Foxm1b were elevated in Nfkb1−/− mice, compared with WT. Deletion of Nfkb1 was associated with an increase in gene expression of Nkx2-5 and of Tbx20. Cardiac mRNA levels of the cardioprotective proteins brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) were quantified. BNP expression was increased in the Nfkb1−/− mice, compared with WT; however, expression of ANP was barely detectable in Nfkb1−/− mice. RLTD was calculated between WT and Nfkb1−/− mice and expressed as mean fold change ± SEM, relative to WT; n = 5 mice/genotype. Original magnification, ×400. Scale bars: 100 μm.