Skip to main content
. Author manuscript; available in PMC: 2013 May 1.
Published in final edited form as: J Mol Cell Cardiol. 2012 Feb 3;52(5):1135–1144. doi: 10.1016/j.yjmcc.2012.01.021

Figure 1.

Figure 1

Post-MI induction of NF-κB and inflammatory gene expression in MyD88−/− hearts. (A) Schematic of transgenically expressed NF-κB activity reporter construct (upper panel). Luciferase activity from heart lysates from NF-κB reporter mice 1 and 7 days after MI were determined. Luciferase activity was normalized to the protein content of the lysates (n≥3 mice/group). (B) RNA from control (Ctr) and post-MI (1week and 3 week) WT and MyD88−/− hearts was isolated and mRNA for (B) complement factor B (Cfb), (C) TNF-α (Tnfa), and (D) chemokine Cxcl10 (Cxcl10) were quantified using qPCR (ΔΔCT method). Gapdh mRNA expression was used as a loading control (n=3 hearts per group). One-way ANOVA with Bonferroni’s post-test (*** P ≤ 0.0001, * P ≤ 0.01, n.s. = not significant).