1992 Fiscal Year Final Research Report Summary
Interactions of intracellular messengers of amylase secretion in pancreatic acini
| Project/Area Number |
03670356
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | Nagoya University |
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Principal Investigator |
HAYAKAWA Tetsuo Nagoya University School of Medicine, Assistant Professor, 医学部, 講師 (80022838)
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| Project Period (FY) |
1991 – 1992
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| Keywords | exocrine secretion / pancreatic acini / intracellular messengers / permeabilized cell / calmodulin / calmodulin kinase / W7 / KN62 |
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| Research Abstract |
To investigate the interactions of intracellular messengers of amylase secretion in stimulus-secretion coupling in pancreatic acini, we studied the effects of A23187, TPA,dbcAMP on amylase secretion. These experiments reveal that Ca^<2+> plays a crucial role in the interactions of intracellular mediators. Then we studied the effect of W7, a calmodulin inhibitor, and KN62, a specific inhibitor of calmodulindependent protein kinase II, on amylase secretion to investigate the role of calmodulin and calmodulin-dependent kinase in Ca^<2+>-dependent amylase secretion. W7 and KN62 reduced amylase secretion stimulated by CCK. W7 and KN62 did not inhibit amylase secretion stimulated by A23187 or TPA, but reduced a synergistic secretion by both A23187 and TPA. W7 and KM62 had no effects on Ca^<2+>-dependent amylase secretion from permeabilized acini, but inhibited the enhancement of Ca^<2+>-dependent amylase secretion by GTPyS, TPA or cAMP. These data suggest that calmodulin plays an important role in Ca^<2+>-dependent amylase secretion from pancreatic acinar cells and in the interactions between Ca^<2+> and other intracellular messengers.
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