NDLI: ATP depletion inhibits Ca2+ release, influx and extrusion in pancreatic acinar cells but not pathological Ca2+ responses induced by bile

Content Provider	Springer Nature Link
Author	Barrow, Stephanie L. Voronina, Svetlana G. Silva Xavier, Gabriela Chvav, Misha A. Longbottom, Rebecca E. Gerasimenko, Oleg V. Petersen, Ole H. Rutter, Guy A. Tepikin, Alexei V.
Copyright Year	2007
Abstract	Here, we describe novel mechanisms limiting a toxic cytosolic Ca2+ rise during adenosine 5′-triphosphate (ATP) depletion. We studied the effect of ATP depletion on Ca2+ signalling in mouse pancreatic acinar cells. Measurements of ATP in isolated cells after adenovirus-mediated expression of firefly luciferase revealed that the cytosolic ATP concentration fell from approximately 1 mM to near zero after treatment with oligomycin plus iodoacetate. ATP depletion resulted in the inhibition of Ca2+ extrusion, which was accompanied by a remarkably synchronous inhibition of store-operated Ca2+ influx. Alternative inhibition of Ca2+ extrusion by carboxyeosin had a much smaller effect on Ca2+ influx. The coordinated metabolic inhibition of Ca2+ influx and extrusion suggests the existence of a common ATP-dependent master regulator of both processes. ATP-depletion also suppressed acetylcholine (ACh)-induced Ca2+ oscillations, which was due to the inhibition of Ca2+ release from internal stores. This could be particularly important for limiting Ca2+ toxicity during periods of hypoxia. In contrast, metabolic control of Ca2+ influx and Ca2+ release from internal stores spectacularly failed to prevent large toxic Ca2+ responses induced by bile acids—activators of acute pancreatitis (a frequent and often fatal disease of the exocrine pancreas). The bile acids taurolithocholic acid 3-sulphate (TLC-S), taurochenodeoxycholic acid (TCDC) and taurocholic acid (TC) were used in our experiments. Neither Ca2+ release from internal stores nor Ca2+ influx triggered by bile acids were inhibited by ATP depletion, emphasising the danger of these pathological mechanisms.
Starting Page	1025
Ending Page	1039
Page Count	15
File Format	PDF
ISSN	00316768
Journal	Pflügers Archiv
Volume Number	455
Issue Number	6
e-ISSN	14322013
Language	English
Publisher	Springer-Verlag
Publisher Date	2007-10-20
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Calcium signalling Calcium influx Pancreas ATP Calcium release Human Physiology
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Clinical Biochemistry

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