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. 2014 Jan 30;306(7):G557–G574. doi: 10.1152/ajpgi.00153.2013

Fig. 6.

Fig. 6.

Dkk1 promotes cellular senescence. A: percentage of senescence-associated β-galactosidase (SA-β-Gal)-positive EPC2 cells before (untreated) and after treatment with rhDkk1 (left). Values are means ± SE of ≥500 cells of ≥3 independent biological replicates. *P ≤ 0.05. Right: SA-β-Gal staining in EPC2 cells before and after treatment with rhDkk1. Arrowheads, SA-β-Gal-positive cells. B: quantitative RT-PCR analysis of p16, p21, Ki-67, and cyclin D1 mRNA levels in EPC2 cells treated with rhDkk1. Data were normalized to β-actin expression. Values are means ± SE of 3 independent experiments. *P ≤ 0.05 vs. untreated. C: Western blot analysis of phosphorylated (Ser780) retinoblastoma (Rb), p53, p21, and p16 protein expression in untreated and rhDkk1-treated EPC2 cells. β-Actin served as loading control. Blots represent results from 3 experiments.