Ethanol modifies the actin cytoskeleton in rat pancreatic acinar cells--comparison with effects of CCK
| Autor: | Frank Lüthen, Eva Siegmund, Heike Weber, Johanna Kunert |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
Pancreatic acinar cells
medicine.medical_specialty Endocrinology Diabetes and Metabolism Filamentous actin Sincalide chemistry.chemical_compound Internal medicine medicine Animals Enzyme Inhibitors Pancreas Cytoskeleton Protein Kinase C Cholecystokinin Ethanol Hepatology L-Lactate Dehydrogenase business.industry Gastroenterology Actin cytoskeleton Actins Cell biology Rats Coupling (electronics) Enzyme Activation Endocrinology chemistry Rats Inbred Lew Alcoholic pancreatitis Tetradecanoylphorbol Acetate Female alpha-Amylases business |
| Zdroj: | Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]. 4(1) |
| ISSN: | 1424-3903 |
| Popis: | One of the early events leading to alcoholic pancreatitis seems to be the effect of ethanol on stimulus-secretion coupling. This study examines ethanol-induced modifications of filamentous actin (F-actin) content and localization in acini, the resulting alpha-amylase secretion and the role of protein kinase C (PKC) activity in these processes.Freshly isolated acini were treated with different concentrations of ethanol or cholecystokinin octapeptide (CCK-8) for different periods. F-actin was localized by confocal laser scanning microscopy; its quantity was determined fluorometrically, and the alpha-amylase secretion was measured.Ethanol caused F-actin reorganization resembling the effects of supramaximal CCK-8 stimulation and of direct PKC activation by phorbol-12-myristate-13-acetate. The polyphasic time course of the F-actin content also resembled that under supramaximal CCK-8 stimulation and was counteracted by inhibition of PKC. The PKC inhibitor bisindolylmaleimide I did not increase the ethanol- induced alpha-amylase secretion, but the suboptimally CCK-8-stimulated secretion via high-affinity receptors.Ethanol, like supramaximal CCK-8 concentrations, inhibits acinar secretion by reorganization of the actin cytoskeleton via PKC activation. This effect is suggested to be mediated by low-affinity CCK-A receptors. Together with the ethanol-induced stimulation of early steps of stimulus-secretion coupling, this may be a pancreas-damaging mechanism resembling that in experimental hyperstimulation pancreatitis. |
| Databáze: | OpenAIRE |
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