Fig. 2.

11Beta-dichloro ameliorates cystic disease in the adult Pax8 model of PKD by inducing apoptosis in cystic cells. (A) Representative whole kidney H&E scans of wild-type (Left), vehicle-treated (Middle), and 11beta-dichloro-treated (Right) kidneys. (Scale bar, 1 mm.) Morphological—(B) two kidney/body weight ratio and (C) cystic index—and functional parameters—(D) BUN and (E) creatinine—show that 11beta-dichloro treatment improved disease progression compared with vehicle-treated mice (n = 7 for wild-type and n = 8 for vehicle- and 11beta-dichloro-treated cystic groups). (F) Apoptosis was evaluated by TUNEL staining in cyst lining epithelia from both distal (DBA positive) and proximal (LTA positive) regions of the nephron. Compared with vehicle, 11beta-dichloro increased apoptosis in both regions of the nephron in Pkd1^−/− animals. (Scale bar, 20 µm.) (G) Quantitation of the apoptotic index from (F), three kidneys from three mice per experimental condition, >1,000 DBA-positive or LTA-positive cells were counted for each sample. The apoptosis markers (H) cleaved PARP and (I) cleaved caspase three were increased in the 11beta-dichloro-treated vs. vehicle-treated kidneys as seen by immunoblotting. Statistics: **P < 0.01; ***P < 0.001 determined by ANOVA (B–E) or t test (G). Data are plotted as mean ± SEM.