Functional Coupling Between the Cyclic Adenosine Monophosphate Pathway and Cholecystokinin Secretion in RIN Cells
Autor: | J. Philippe, JC Cuber, S. Aucouturier, C. Roche, J. A. Chayvialle, C. Bernard |
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Přispěvatelé: | ProdInra, Migration, Unité de recherche d'Écologie et Physiologie du Système Digestif (UEPSD), Institut National de la Recherche Agronomique (INRA) |
Rok vydání: | 1994 |
Předmět: |
medicine.medical_specialty
Thapsigargin Calmodulin Biophysics AMP CYCLIQUE In Vitro Techniques digestive system Biochemistry chemistry.chemical_compound Internal medicine [SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular Biology Cyclic AMP Tumor Cells Cultured medicine Animals [SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology Cyclic adenosine monophosphate Protein kinase A Protein Kinase Inhibitors Molecular Biology Cholecystokinin Forskolin biology Voltage-dependent calcium channel Calcium channel Colforsin digestive oral and skin physiology Cell Biology Adenoma Islet Cell Rats Endocrinology chemistry Calcium-Calmodulin-Dependent Protein Kinases biology.protein RAT Calcium hormones hormone substitutes and hormone antagonists |
Zdroj: | Biochemical and Biophysical Research Communications Biochemical and Biophysical Research Communications, Elsevier, 1994, 200 (3), pp.1382-1390 |
ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1006/bbrc.1994.1604 |
Popis: | The cellular events associated with cAMP-dependent cholecystokinin (CCK) release were investigated with an X-ray induced rat pancreatic tumor cell line (RIN 1056 E). Forskolin dose-dependently stimulated the release of CCK. Agents that increase [Ca2+]i (thapsigargin, Bay K 8644, ionomycin) also stimulated the release of CCK. Conversely, absence of extracellular Ca2+ or cell treatment with various calcium channel blockers strongly reduced the forskolin-induced CCK release. Finally, the cAMP-kinase inhibitor H89, the calmodulin antagonist W7 and the Ca/calmodulin-dependent protein-kinase II inhibitor KN62 strongly inhibited the forskolin-evoked CCK secretion. We conclude that the release of CCK via a cAMP-dependent pathway is dependent on the activation of voltage-dependent calcium channels and may implicate protein kinase A, calmodulin and the Ca/calmodulin-dependent protein kinase II. |
Databáze: | OpenAIRE |
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