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Originally published In Press as doi:10.1194/jlr.M500180-JLR200 on October 13, 2005

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Journal of Lipid Research, Vol. 47, 32-41, January 2006
Copyright © 2006 by American Society for Biochemistry and Molecular Biology

Gallbladder histopathology during murine gallstone formation: relation to motility and concentrating function

Karel J. van Erpecum1,2,*, David Q-H. Wang1,{dagger}, Antonio Moschetta§, Domenico Ferri**, Maria Svelto{dagger}{dagger}, Piero Portincasa§§, Jan-Jaap Hendrickx***, Marguérite Schipper*** and Giuseppe Calamita{dagger}{dagger}

* Department of Gastroenterology, University Medical Center Utrecht, Utrecht, The Netherlands
{dagger} Gastroenterology Division, Beth Israel Deaconess Medical Center, Harvard Medical School, and Harvard Digestive Diseases Center, Boston, MA
§ Howard Hughes Medical Institute and Department of Pharmacology, University of Texas Southwestern Medical Center, Dallas, TX
** Department of Zoology, Laboratory of Histology and Comparative Anatomy, University of Bari, Bari, Italy
{dagger}{dagger} Department of General and Environmental Physiology, University of Bari, Bari, Italy
§§ Section of Internal Medicine, Department of Internal and Public Medicine, University of Bari, Bari, Italy
*** Department of Pathology, University Medical Center Utrecht, Utrecht, The Netherlands

Published, JLR Papers in Press, October 13, 2005.

1 K. J. van Erpecum and D. Q-H. Wang contributed equally to this work.

2 To whom correspondence should be addressed. e-mail: k.j.vanerpecum{at}azu.nl

C57L mice are susceptible and AKR mice are resistant to gallstone formation. We studied in male mice of both strains gallbladder histopathology, cholecystokinin-induced emptying, and concentrating function at 0, 14, 28, and 56 days on a lithogenic diet. Gallbladder wall thickness increased on the diet, with stromal granulocyte infiltration, progressive fibrosis, edema, and epithelial cell indentation, particularly in C57L. Strong basal cholecystokinin octapeptide-induced gallbladder emptying (70% of fasting volumes) occurred in both strains, but fasting gallbladder volumes were significantly larger in C57L (14.8 ± 2.2 µl vs. 8.8 ± 1.0 µl). On the diet, fasting volumes increased exclusively in C57L (28.6 ± 2.9 µl on day 56), with progressively decreased emptying (27% of fasting volumes on day 56). Gallbladder emptying remained normal in AKR. Gallbladder concentrating function decreased on the lithogenic diet (especially in C57L), coinciding with decreased aquaporin-1 (AQP1) and AQP8 expression at the mRNA and protein levels. In additional experiments, similar downregulation of AQP1 and AQP8 mRNA expression occurred in farnesoid X receptor (FXR)-deficient mice after 1 week on the lithogenic diet, without any difference from corresponding wild-type mice. In conclusion, during murine lithogenesis, altered gallbladder histology is associated with impaired motility, reduced concentrating function, and decreased AQP1 and AQP8 expression, the latter without the involvement of the FXR.

Supplementary key words aquaporin • cholesterol • farnesoid X receptor • gallbladder emptying • water channel

Abbreviations: CCK, cholecystokinin octapeptide; FXR, farnesoid X receptor


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