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Additional file 1: Figure S1. X-ray diffraction pattern of CuFe2O4 impregnated on different structured mesoporous materials. Figure S2. Nitrogen adsorption-desorption isotherm of CuFe2O4 impregnated on different structured mesoporous materials (a) CuFe2O4/Q-10 silica, (b) CuFe2O4/SBA-16, (c) CuFe2O4/Hydrophobic silica, (d) CuFe2O4/MesoZSM-5, (e) CuFe2O4/Mesobeta. Figure S3. Pore size distributions of CuFe2O4 impregnated on different structured mesoporous materials (a) CuFe2O4/Q-10 silica, (b) CuFe2O4/SBA-16, (c) CuFe2O4/Hydrophobic silica, (d) CuFe2O4/MesoZSM-5, (e) CuFe2O4/Mesobeta. Figure S4. Vibrating sample magnetometer analysis of (a) CuFe2O4/MCM-41 and (b) CuFe2O4/Mesosilicalite. Table S1. Textural characteristics of 30% CuFe2O4 impregnated on different mesostructured materials. Table S2. Descriptive statistics of curcumin release over different CuFe2O4/structured silica based nanoformulations. Table S3. Curcumin release over different CuFe2O4/structured silica based nanoformulations (One way ANOVA). Table S4. Post hoc tests for mean difference in curcumin release among different CuFe2O4/structured silica based nanoformulations. Table S5. Pearson correlation of curcumin release over different CuFe2O4/structured silica based nanoformulations. Table S6. Statistical analysis of the cell viability assay performed on (A) MCF7, (B) HeLa, (C) HCT116, and (D) HFF cell lines. Analysis of drug treated was performed compared to cell control (without treatment) using 2way ANOVA with Dunnett���s post hoc test. *p

© 2015 the American Physiological Society. Intestinal epithelial cell renewal relies on the right balance of epithelial cell migration, proliferation, differentiation, and apoptosis. Intestinal epithelial cells consist of absorptive and secretory lineage. The latter is comprised of goblet, Paneth, and enteroendocrine cells. Fibroblast growth factor 10 (FGF10) plays a central role in epithelial cell proliferation, survival, and differentiation in several organs. The expression pattern of FGF10 and its receptors in both human and mouse intestine and their role in small intestine have yet to be investigated. First, we analyzed the expression of FGF10, FGFR1, and FGFR2, in the human ileum and throughout the adult mouse small intestine. We found that FGF10, FGFR1b, and FGFR2b are expressed in the human ileum as well as in the mouse small intestine. We then used transgenic mouse models to overexpress Fgf10 and a soluble form of Fgfr2b, to study the impact of gain or loss of Fgf signaling in the adult small intestine. We demonstrated that overexpression of Fgf10 in vivo and in vitro induces goblet cell differentiation while decreasing Paneth cells. Moreover, FGF10 decreases stem cell markers such as Lgr5, Lrig1, Hopx, Ascl2, and Sox9. FGF10 inhibited Hes1 expression in vitro, suggesting that FGF10 induces goblet cell differentiation likely through the inhibition of Notch signaling. Interestingly, Fgf10 overexpression for 3 days in vivo and in vitro increased the number of Mmp7/Muc2 double-positive cells, suggesting that goblet cells replace Paneth cells. Further studies are needed to determine the mechanism by which Fgf10 alters cell differentiation in the small intestine.