Skip to main content
. 2013 Feb 20;133(1):42–53. doi: 10.1093/toxsci/kft027

Fig. 6.

Fig. 6.

TCDD inhibits the downstream canonical WNT target LEF1, and RSPOs fully restore LEF1. E14.5 male UGSs were cultured for 4 days in DHT (10nM) containing media. Supplements to the media were either vehicle (0.1% DMSO) or TCDD (1nM) and RSPO2 and/or RSPO3 (100ng/ml each). Treatment groups were vehicle, TCDD, RSPO2 + TCDD, RSPO3 + TCDD, and RSPO2 + RSPO3 + TCDD. Near mid-sagittal sections (5 µm) were immunostained for LEF1 and counterstained for KRT14 to mark BE cells, which are the site of prostatic bud formation. Nuclei were stained with DAPI. Large boxes indicate enlarged images (200×) of small box areas in each sample to demonstrate colocalization of LEF1 and KRT14 in BE cells. Arrows indicate cells positive for LEF1/KRT14. Percent of BE cells positive for LEF1 was determined by counting the number of BE cells positive for LEF1 in the entire UGS and dividing that number by the total number of BE cells. Results are mean ± SE of at least four litter-independent UGSs per treatment. Asterisk denotes a significant difference compared with vehicle, whereas a cross indicates a significant difference compared with TCDD (p < 0.05).