Skip to main content
. 2019 Dec 16;318(3):F817–F825. doi: 10.1152/ajprenal.00436.2019

Fig. 3.

Fig. 3.

Analysis of the role of β-catenin pathway in the regulation of α-epithelial Na+ channel (ENaC) expression in response to histidine-tagged soluble (pro)renin receptor (sPRR-His) treatment. Primary rat inner medullary collecting duct cells were pretreated with the β-catenin inhibitor ICG-001 (ICG) at 10 μM or OMP54F03 (OMP) at 10 μM for 1 h and then treated with 10 nM sPRR-His for 24 h. α-ENaC protein and mRNA were determined by immunoblot analysis (A and B) and quantitative RT-PCR (C and D), respectively. A: effect of ICG on increased α-ENaC protein expression induced by sPRR-His. B: effect of OMP on increased α-ENaC protein expression induced by sPRR-His. C: effect of ICG on increased α-ENaC mRNA induced by sPRR-His. D: effect of OMP on increased α-ENaC mRNA induced by sPRR-His. mpkCCD cells were transfected with a construct expressing luciferase under the control of a flanking region of α-ENaC or empty plasmid (E). The transfected cells were pretreated with ICG at 10 μM or OMP at 10 μM for 1 h and then treated with vehicle or 10 nM sPRR-His for 24 h. Cells were lyzed and assayed for luciferase activity. Data are means ± SE; n = 4–5 per group for A–D and n = 9–10 per group for E. *P < 0.05 vs. control (CTR); #P < 0.05 vs. sPRR-His treatment.