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. 2018 May 22;9(39):25572–25585. doi: 10.18632/oncotarget.25385

Figure 3. Experimental design and effects of FGF15 deficiency on colon epithelial cell proliferation in AOM/DSS-treated mice.

Figure 3

(A) Experimental design and mouse weights over the course of the 20-week study. We weighed mice weekly. Vertical arrows on the horizontal axis indicate intraperitoneal injection with 7.5 mg/kg AOM/kg body weight at day 1, 8, 15, and 22. Vertical blue band indicates that we added 2.5% dextran sulfate sodium (DSS) to the drinking water of AOM-treated mice on days 29 through 33. Fourteen WT and 15 Fgf15-/- mice were treated with AOM plus DSS. Error bars denote SE. There were no differences between the weights of WT and FGF15-deficient mice. However, regardless of genotype, male mice weighed 10-20% more than female mice. (B and C) Representative images of Ki67 immunostaining in crypts from female and male WT (B) and Fgf15-/- (C) mouse colons. Note increased Ki67 immunostaining in upper portions of crypts from FGF15-deficient mice. (D-F) FGF15 deficiency is associated with increased colon epithelial cell proliferation. An investigator masked to genotype measured the Ki67 labeling index in normal crypts from the distal half of each mouse colon. Crypts were divided into five equal zones, starting from the proliferative area at the base (zone 1) and extending to the luminal surface (zone 5), and immunostaining was assessed in approximately 1000 colon epithelial cells from each mouse. (D) Results for 14 WT and 15 Fgf15-/- mice; (E) Results for 6 WT and 7 Fgf15-/- female mice; (F) Results for 8 WT and 8 Fgf15-/- male mice. We observed significant increases in Ki67 staining in the upper portions of crypts in non-neoplastic segments of colon from FGF15-deficient compared to WT mice overall and in female and male mice evaluated separately. (***P < 0.001).