Research Paper Volume 14, Issue 10 pp 4281—4304

Figure 4. AhR modulates the senescence-associated secretory phenotype with aging. (A). Chromatin immunoprecipitation (ChIP) for AhR binding to XRE binding sites located in the promoters of p16^Ink4a (A), p21^Cip1 (B) and TNFα (C). qPCR was used to quantify changes in DNA binding and the results were normalized to the corresponding inputs. Amounts of MCP-2 (D), MMP12 (E), FGF (F) and HGF (G) were analyzed in liver homogenates from AhR+/+ and AhR−/− mice at the indicated ages. Levels of HGF (H) and VEGF (I) VEGF were also determined in sera from mice of the same genotypes and ages. Bio-Plex Multiplex immunoassays kits were used. Oligonucleotides for qPCR are indicated in Supplementary Table 1. Gapdh was used to normalize target gene expression (△Ct) and 2^−△△Ct to calculate changes in mRNA levels with respect to wild type or untreated conditions. Data are shown as mean + SD (^*P < 0.05; ^**P < 0.01; ^***P < 0.001).