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

Figure 4.

Figure 4

p50 suppresses the prohypertrophic effects of c-Rel. H9c2 cells were transiently transfected with expression plasmids (control RSV-β-gal, RSV-p50, or RSV-c-Rel). RNA was isolated, and cDNA was generated and used as a template for qRT-PCR. The RLTD was calculated and expressed as mean fold change ± SEM, relative to RSV, of five independent transfections. A: Gene expression levels of the individual NF-κB subunits revealed that overexpression of p50 repressed expression of c-Rel. B: RNA was isolated from the hearts of adult WT and Nfkb1−/− mice, and mRNA levels of the NF-κB subunits RelA, NF-κB2, c-Rel, and RelB were quantified using qRT-PCR. c-Rel was the only NF-κB subunit to be up-regulated in Nfkb1−/− mice. The RLTD between WT and Nfkb1−/− mice was calculated and expressed as a mean fold change ± SEM relative to WT; n = 5 mice/genotype. *P = 0.05, **P = 0.01. C: Representative photographs of hearts isolated from adult WT and Nfkb1−/− mice show increased heart size in Nfkb1−/− mice. D: The heart/body weight ratio was calculated in Nfkb1−/− and WT control mice on a pure C57Bl/6 background; data are expressed as mean percentage change ± SEM, compared with WT; n = 17 mice/genotype. An increase in heart/body weight ratio was observed in male Nfkb1−/− mice, compared with WT controls, in both backgrounds. ***P < 0.001.