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©2006 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Jun 14, 2006; 12(22): 3466-3470
Published online Jun 14, 2006. doi: 10.3748/wjg.v12.i22.3466
Published online Jun 14, 2006. doi: 10.3748/wjg.v12.i22.3466
Calcium signaling in cholangiocytes
Noritaka Minagawa, Barbara E Ehrlich, Departments of Medicine and Pharmacology Yale University School of Medicine, New Haven, CT, United States
Michael H Nathanson, Section of Digestive Diseases, Yale University School of Medicine, 1 Gilbert Street, Room TAC S241D, New Haven, CT 06519, United States
Author contributions: All authors contributed equally to the work.
Supported by NIH grants DK61747, DK45710, DK57751, and DK34989, and by a grant-in-aid from the American Heart Association
Correspondence to: Michael H Nathanson, Section of Digestive Diseases, Yale University School of Medicine, 1 Gilbert Street, Room TAC S241D, New Haven, CT 06519, United States. michael.nathanson@yale.edu
Telephone: +1-203-7857312 Fax: +1-203-7854306
Received: January 1, 2006
Revised: January 14, 2006
Accepted: January 24, 2006
Published online: June 14, 2006
Revised: January 14, 2006
Accepted: January 24, 2006
Published online: June 14, 2006
Abstract
Cytosolic Ca2+ is an important second messenger in virtually every type of cell. Moreover, Ca2+ generally regulates multiple activities within individual cells. This article reviews the cellular machinery that is responsible for Ca2+ signaling in cholangiocytes. In addition, two Ca2+-mediated events in cholangiocytes are discussed: bicarbonate secretion and apoptosis. Finally, emerging evidence is reviewed that Ca2+ signaling is involved in the pathogenesis of diseases affecting the biliary tree and that Ca2+ signaling pathways can be manipulated to therapeutic advantage in the treatment of cholestatic disorders.
Keywords: Ca2+; Cholangiocyte; Inositol trisphosphate; Bile secretion; Cholestasis; Apoptosis