ISSN:
0021-9541
Keywords:
Life and Medical Sciences
;
Cell & Developmental Biology
Source:
Wiley InterScience Backfile Collection 1832-2000
Topics:
Biology
,
Medicine
Notes:
C6 glioma cells possess β adrenergic receptors coupled with adenylate cyclase which can be irreversibly blocked by bromoacetylaminomethylpindolol (Br-AAM-pindolol), a β adrenergic antagonist. With 1 μM Br-AAM-pindolol, more than 80% of β adrenergic receptors, labeled by (3H)-dihydroalprenolol ((3H)-DHA), were blocked. After this blockade, new β adrenergic receptors were synthesized only during cell division. However, at cell confluency when the cell number was constant, turnover of β adrenergic receptors was barely detectable. Cycloheximide (1 μg/ml) inhibited cell growth as well as reappearance of β adrenergic receptors. A 90% loss of β adrenergic receptors in C6 glioma cells was obtained after down-regulation for 15 h with 10 μM isoproterenol, a β adrenergic agonist. After removal of the agonist, recovery of β-adrenergic-sensitive adenylate cyclase was complete within 2 to 3 days, whereas β adrenergic receptors reached 90% of control value within 6 days. The half-life of the receptor recovery was 2 to 3 days. Pretreatment of C6 glioma cells by Br-AAM-pindolol and subsequent cell exposure to isoproterenol indicated that down regulation and recovery of unblocked β adrenergic receptors did occur; however isoproterenol did not accelerate the biosynthesis of β adrenergic receptors. The recovery of both biological response and β adrenergic receptor occupancy was restored both in the presence or absence of cycloheximide (1 μg/ml), a concentration which blocked 90% of protein synthesis. Our results suggest that reappearance of β adrenergic receptors in C6 glioma cells, following isoproterenol-induced down regulation, was not due to synthesis of new receptors but to recycling of the β adrenergic receptors.
Additional Material:
8 Ill.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1002/jcp.1041210318
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