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Pancreatology. 2015 Jul;15(4 Suppl):S44-8. doi: 10.1016/j.pan.2015.05.477. Epub 2015 Jun 12.

Calcium signaling and secretion in cholangiocytes.

Author information

1
Section of Digestive Diseases, Department of Internal Medicine, Yale University School of Medicine, USA.
2
Section of Digestive Diseases, Department of Internal Medicine, Yale University School of Medicine, USA. Electronic address: michael.nathanson@yale.edu.

Abstract

Alcoholic hepatitis affects up to one-third of individuals who abuse alcohol and can be associated with high mortality. Although this disorder is characterized by hepatocellular damage, steatosis and neutrophil infiltration, recent evidence suggests that cholestasis or impaired bile secretion may be a frequent occurrence as well. Bile secretion results from the concerted activity of hepatocytes and cholangiocytes, the epithelial cells that line the bile ducts. Hepatocytes secrete bile acids and conjugated products into the bile canaliculi, which then are modified by cholangiocytes through secretion of bicarbonate and water to give rise to the final secreted bile. Here the molecular mechanisms regulating bile secretion in cholangiocytes are reviewed. Moreover, we discuss how the expression of intracellular Ca(2+) channels might be regulated in cholangiocytes, plus evidence that components of the Ca(2+) signaling machinery are altered in a range of cholestatic diseases of the bile ducts.

KEYWORDS:

Alcoholic hepatitis; Bicarbonate Secretion; Bile ducts; Bile formation; Cholestasis; InsP3 receptors

PMID:
26100660
PMCID:
PMC4603373
DOI:
10.1016/j.pan.2015.05.477
[Indexed for MEDLINE]
Free PMC Article

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