Figure 3.

JDP2 is involved in SFN-induced ARE transactivation. (a) ARE-driven transcriptional activity in WT and Jdp2 KO MEFs after treatment with or without SFN (5 × 10^–6 M) in the presence or absence of 50 nmol/l of CORM. The pGL4–hQR25–luciferase plasmid was transfected into WT and Jdp2 KO MEFs. After 24 h of culture, SFN (5 μM) was added and cells were cultured for an additional 12 h. Cellular luciferase activity was measured (n=3) as described in Materials and Methods. *P<0.05; **P<0.01. (b) Protein detection in WT and Jdp2 KO MEFs treated with SFN. After 24 h of culture, SFN (10 μM) was added and cells were cultured for an additional 12 h. Cellular lysates from WT and Jdp2 KO MEFs (40 μg) were separated on SDS-PAGE and transferred onto membranes, and the antibody specific for each protein of interest was used for immunodetection. (c) Comparison of epidermal thickening induced by TPA and SFN in WT and Jdp2 KO mice. WT and Jdp2 KO mice were painted with acetone or TPA (8.1 nmol in 100 μl of acetone) or SFN (15 nmol in 100 μl of acetone) twice, and skin tissue sections were prepared and stained with hematoxylin and eosin. Each group included five mice. The epidermal thickness of the skin was measured at 10 sites of an area randomly selected and was defined as the distance from the basal layer to the corneal layer. The results for epidermal thickening are quantified in (d) (n=3). *P<0.05; **P<0.01