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Bile acids induce calcium signals in mouse pancreatic acinar cells: implications for bile‐induced pancreatic pathology
Author(s) -
Voronina Svetlana,
Longbottom Rebecca,
Sutton Robert,
Petersen Ole H.,
Tepikin Alexei
Publication year - 2002
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2002.017525
Subject(s) - calcium , bile acid , pancreas , medicine , chemistry , pancreatic juice , pancreatitis , basal (medicine) , endocrinology , biochemistry , biology , insulin
The effect of the natural bile acid, taurolithocholic acid 3‐sulfate (TLC‐S), on calcium signalling in pancreatic acinar cells has been investigated. TLC‐S induced global calcium oscillations and extended calcium transients as well as calcium signals localised to the secretory granule (apical) region of acinar cells. These calcium signals could still be triggered by TLC‐S in a calcium‐free external solution. TLC‐S‐induced calcium signals were not inhibited by atropine, but were abolished by caffeine or by depletion of calcium stores, due to prolonged application of ACh. Global calcium signals, produced by TLC‐S application, displayed vectorial apical‐to‐basal polarity. The signals originated in the apical part and were then propagated to the basal region. Other natural bile acids, taurocholate (TC) and taurodeoxycholate (TDC), were also able to produce local and global calcium oscillations (but at higher concentrations than TLC‐S). Bile, which can enter pancreas by reflux, has been implicated in the pathology of acute pancreatitis. The calcium releasing properties of bile acids suggest that calcium toxicity could be an important contributing factor in the bile acid‐induced cellular damage.