1. Volume 130, Issue 2, Pages 349-358 (February 2006)
Involvement of the Anion Exchanger SLC26A6 in Prostaglandin E2- but not Forskolin- Stimulated Duodenal HCO3− Secretion 
BiGuang Tuo, Brigitte Riederer, Zhaohui Wang, William H. Colledge, Manoocher Soleimani, Ursula Seidler 
Gastroenterology 
Volume 130, Issue 2, Pages (February 2006)
DOI: /j.gastro
Copyright © 2006 American Gastroenterological Association Terms and Conditions

2. Figure 1
Effects of PGE2 (10−6 mol/L), forskolin (10−5 mol/L), and carbachol (10−4 mol/L) on (A) duodenal HCO3− secretion and (B) Isc in SLC26A6−/− mice and their wild-type littermates (SLC26A6+/+). The data shown represent the net maximal increases in HCO3− secretion and Isc observed, and were expressed as the mean ± SEM. In SLC26A6−/−, PGE2-stimulated ΔJHCO3− was strongly reduced by 59% and carbachol-stimulated ΔJHCO3− was reduced by 35%, but both PGE2- and carbachol-stimulated ΔIsc were not altered significantly. No significant changes in forskolin-stimulated ΔHCO3− and ΔIsc were noted (compared with SLC26A6+/+: #, P > .05; ****P < .0001, by Student t tests). ■, SLC26A6+/+ , SLC26A6−/−.
Gastroenterology  , DOI: ( /j.gastro )
Copyright © 2006 American Gastroenterological Association Terms and Conditions

3. Figure 2
Effects of bilateral Cl− removal on PGE2-stimulated (10−6 mol/L), forskolin-stimulated (10−5 mol/L), and carbachol-stimulated (10−4 mol/L) (A) duodenal HCO3− secretory response and (B) Isc. Experiments were performed in white Swiss mice. The data shown represent the net maximal increases in HCO3− secretion and Isc observed, and were expressed as the mean ± SEM. In bilateral Cl−-free solutions, PGE2-stimulated ΔJHCO3− was reduced by 81% and ΔIsc by 88%, and carbachol-stimulated ΔJHCO3− was reduced by 44% and ΔIsc by 74%. Forskolin-stimulated ΔHCO3− was not altered significantly, but forskolin-induced ΔIsc was reduced by 69% (compared with Cl−-containing: #P > .05; ****P < .0001, by Student t tests). ■, Cl− containing; , Cl− free.
Gastroenterology  , DOI: ( /j.gastro )
Copyright © 2006 American Gastroenterological Association Terms and Conditions

4. Figure 3
Effects of only luminal Cl− removal on PGE2-stimulated (10−6 mol/L) (A) duodenal HCO3− secretion and (B) Isc. Identical experiments as in Figure 2, except for selective removal of Cl− from the luminal bath. The data shown represent the net maximal increases in HCO3− secretion and Isc observed, and were expressed as the mean ± SEM. PGE2-stimulated ΔJHCO3− was reduced by 69% in only luminal Cl−-free solution, but ΔIsc was not altered significantly (compared with Cl−-containing: #P > .05; ****P < .0001, by Student t tests). ■, Cl− containing; , luminal Cl− free.
Gastroenterology  , DOI: ( /j.gastro )
Copyright © 2006 American Gastroenterological Association Terms and Conditions

5. Figure 4
Effects of CFTR knockout on (A) basal duodenal HCO3− secretion and (B) Isc. Experiments were performed in CFTR knockout mice (CFTR−/−) and their wild-type littermates (CFTR+/+). The data were expressed as the mean ± SEM. In CFTR−/−, basal HCO3− secretion and Isc were reduced by 37% and 44%, respectively. Bilateral Cl− removal induced a greater reduction by 51% in basal HCO3− secretion in CFTR−/− (compared with CFTR+/+: *P < .05; **P < .01, by 1-way ANOVA with the Student–Newman–Keul post hoc test). ■, CFTR+/+ , CFTR−/−; , CFTR−/− and Cl− free.
Gastroenterology  , DOI: ( /j.gastro )
Copyright © 2006 American Gastroenterological Association Terms and Conditions

6. Figure 5
Effects of PGE2 (10−6 mol/L), forskolin (10−5 mol/L), and carbachol (10−4 mol/L) on (A) duodenal HCO3− secretion and (B) Isc in CFTR knockout mice (CFTR−/−) and their wild-type littermates (CFTR+/+). The data shown represent the net maximal increases in HCO3− secretion and Isc observed, and were expressed as the mean ± SEM. In CFTR−/− duodenum, PGE2 stimulated ΔJHCO3− by 71% of the response observed in CFTR+/+ tissue and carbachol stimulated ΔJHCO3− by 48% of the response observed in CFTR+/+ tissue, but both had no significant effects on Isc. After bilateral Cl− removal, PGE2 did not stimulate HCO3− secretion significantly in CFTR−/−. In contrast, forskolin did not significantly stimulate HCO3− and Isc in CFTR−/− (compared with CFTR+/+: *P < .05; ***P < .001; ****P < .0001; compared with CFTR−/− + Cl−-free: a***P < .001, by 1-way ANOVA with the Student–Newman–Keul post hoc test in the PGE2 group, by Student t tests in other groups). ■, CFTR+/+ , CFTR−/−; , CFTR−/− and Cl− free.
Gastroenterology  , DOI: ( /j.gastro )
Copyright © 2006 American Gastroenterological Association Terms and Conditions

7. Figure 6
Semiquantitative reverse-transcription PCR analysis of Slc26a6 mRNA in duodenal mucosa of CFTR−/− mice and their wild-type littermates, with the epithelial marker cytokeratin-18 as the control gene. (A) Representative traces showing the similar amplification efficiency of SLC26A6 and the control gene cytokeratin 18. (B) Expression levels of SLC26A6 in CFTR−/− (n = 3) and their wild-type littermates (n = 3). The ratio of SLC26A6/cytokeratin 18 was calculated from the exponential phase of the amplification (parallel part of the graph, in the case of the shown graph, at cycles 18–20) as described previously in Rossmann et al.28 It shows no significant change in SLC26A6 mRNA expression in the absence of duodenal CFTR expression (compared with CFTR+/+: #P > .05, by Student t test).
Gastroenterology  , DOI: ( /j.gastro )
Copyright © 2006 American Gastroenterological Association Terms and Conditions