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Int J Mol Sci. 2018 Dec 6;19(12). pii: E3913. doi: 10.3390/ijms19123913.

Calcium Signaling in Cholangiocytes: Methods, Mechanisms, and Effects.

Author information

1
Section of Digestive Diseases, Department of Internal Medicine, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520-8019, USA. michele.rodrigues@yale.edu.
2
Section of Digestive Diseases, Department of Internal Medicine, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520-8019, USA. dawidson.gomes@yale.edu.
3
Department of Biochemistry and Immunology, Federal University of Minas Gerais. Av. Antônio Carlos, 6627, Belo Horizonte-MG 31270-901, Brazil. dawidson.gomes@yale.edu.
4
Section of Digestive Diseases, Department of Internal Medicine, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520-8019, USA. michael.nathanson@yale.edu.

Abstract

Calcium (Ca2+) is a versatile second messenger that regulates a number of cellular processes in virtually every type of cell. The inositol 1,4,5-trisphosphate receptor (ITPR) is the only intracellular Ca2+ release channel in cholangiocytes, and is therefore responsible for Ca2+-mediated processes in these cells. This review will discuss the machinery responsible for Ca2+ signals in these cells, as well as experimental models used to investigate cholangiocyte Ca2+ signaling. We will also discuss the role of Ca2+ in the normal and abnormal regulation of secretion and apoptosis in cholangiocytes, two of the best characterized processes mediated by Ca2+ in this cell type.

KEYWORDS:

Ca2+; biliary tree; cholangiocytes; inositol 1,4,5-trisphosphate (InsP3); inositol 1,4,5-trisphosphate receptors (ITPRs); secretion

PMID:
30563259
PMCID:
PMC6321159
DOI:
10.3390/ijms19123913
[Indexed for MEDLINE]
Free PMC Article

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