TY - JOUR
T1 - Inositol trisphosphate-independent agonist-stimulated calcium influx in rat pancreatic acinar cells
AU - Dawra, R. K.
AU - Saluja, A. K.
AU - Runzi, M.
AU - Steer, M. L.
N1 - Copyright:
Copyright 2004 Elsevier B.V., All rights reserved.
PY - 1993
Y1 - 1993
N2 - CCK-JMV-180 is a cholecystokinin analog that stimulates digestive enzyme secretion from pancreatic acinar cells but does not cause either generation of inositol 1,4,5-trisphosphate or depletion of the inositol 1,4,5- trisphosphate-sensitive intracellular Ca2+ storage pool. We report that CCK-JMV-180 can accelerate Ca2+ influx into fura-2-loaded dispersed rat pancreatic acini and single acinar cells. Furthermore, CCK-JMV-180 accelerates Ca2+ influx into cells microinjected with the inositol 1,4,5- trisphosphate receptor antagonist heparin and into acini loaded with the Ca2+-chelating agent BAPTA (1,2-bis(2-aminophenoxy)ethane-N,N,N',N'- tetraacetic acid). These results indicate that agonist-stimulated Ca2+ influx can occur (a) without depletion of the inositol 1,4,5-trisphosphate- sensitive intracellular Ca2+ storage pool, (b) without a rise in cytoplasmic free Ca2+ concentrations, and (c) after blockade of inositol 1,4,5-trisphosphate receptors. They suggest that depletion of an inositol 1,4,5-trisphosphate-independent intracellular Ca2+ storage pool and/or generation of a non-inositol 1,4,5-trisphosphate second messenger by CCK- JMV-180 may be a sufficient signal for acceleration of Ca2+ influx into rat pancreatic acinar cells.
AB - CCK-JMV-180 is a cholecystokinin analog that stimulates digestive enzyme secretion from pancreatic acinar cells but does not cause either generation of inositol 1,4,5-trisphosphate or depletion of the inositol 1,4,5- trisphosphate-sensitive intracellular Ca2+ storage pool. We report that CCK-JMV-180 can accelerate Ca2+ influx into fura-2-loaded dispersed rat pancreatic acini and single acinar cells. Furthermore, CCK-JMV-180 accelerates Ca2+ influx into cells microinjected with the inositol 1,4,5- trisphosphate receptor antagonist heparin and into acini loaded with the Ca2+-chelating agent BAPTA (1,2-bis(2-aminophenoxy)ethane-N,N,N',N'- tetraacetic acid). These results indicate that agonist-stimulated Ca2+ influx can occur (a) without depletion of the inositol 1,4,5-trisphosphate- sensitive intracellular Ca2+ storage pool, (b) without a rise in cytoplasmic free Ca2+ concentrations, and (c) after blockade of inositol 1,4,5-trisphosphate receptors. They suggest that depletion of an inositol 1,4,5-trisphosphate-independent intracellular Ca2+ storage pool and/or generation of a non-inositol 1,4,5-trisphosphate second messenger by CCK- JMV-180 may be a sufficient signal for acceleration of Ca2+ influx into rat pancreatic acinar cells.
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M3 - Article
C2 - 8376384
AN - SCOPUS:0027198007
SN - 0021-9258
VL - 268
SP - 20237
EP - 20242
JO - Journal of Biological Chemistry
JF - Journal of Biological Chemistry
IS - 27
ER -