Mechanisms for the emergence of catecholamine-sensitive adenylate cyclase and β-adrenergic receptors in cultured hepatocytes
| Autor: | Øyvind Melien, Dagny Sandnes, Thoralf Christoffersen, Tor-Erik Sand, S. Jacobsen, Magne Refsnes |
|---|---|
| Rok vydání: | 1983 |
| Předmět: |
Male
medicine.medical_specialty Biophysics Iodocyanopindolol Adenylate kinase Biology Cycloheximide Biochemistry Cyclase Dexamethasone chemistry.chemical_compound Structural Biology Internal medicine Receptors Adrenergic beta Genetics medicine Animals Insulin Adenylate cyclase Testosterone Molecular Biology Cells Cultured Primary culture Isoproterenol Cell Biology Ligand (biochemistry) Rats Thyroxine Endocrinology Liver β-Adrenergic receptor chemistry Protein Biosynthesis Dactinomycin Catecholamine RNA Actinomycin D Cyanopindolol Cyclase activity Rat hepatocyte Adenylyl Cyclases medicine.drug |
| Zdroj: | FEBS Letters. 164:291-298 |
| ISSN: | 0014-5793 |
| DOI: | 10.1016/0014-5793(83)80304-4 |
| Popis: | Adult male rat hepatocytes, which normally respond poorly to beta-adrenergic agents, acquire such responsiveness during primary monolayer culture. We here show that the rise in catecholamine-sensitive adenylate cyclase activity in hepatocytes in vitro is closely paralleled by an increase in the ability to bind the beta-adrenoceptor ligand [125I]cyanopindolol. The emergence of beta-adrenergic responsiveness did not require cell attachment or serum. Addition of dexamethasone, insulin, thyroxine or dihydrotestosterone to the cultures, singly or in combination, did not prevent the augmented beta-adrenergic responsiveness. The increase in catecholamine-sensitive adenylate cyclase activity and [125I]cyanopindolol binding could be blocked by cycloheximide or actinomycin D. Exposure of the cultures to isoproterenol at 3-hourly intervals led to a dose-dependent suppression of the rise in isoproterenol-responsive adenylate cyclase and prevented the increase in beta-adrenoceptor binding. |
| Databáze: | OpenAIRE |
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