Document Detail


Analysis by cell hybridization of mechanisms that regulate beta-adrenergic responses in reticulocytes and in differentiating erythroid cells.
MedLine Citation:
PMID:  1648565     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In intact reticulocytes, but not in fragmented membranes, the loss of adenylate cyclase activity during cell maturation followed a biphasic time course. A rapid phase (t1/2 approximately 2 h) during which the initial activity was reduced by 40-50% was followed by a slow phase with t1/2 close to 3 days. The fast decay seemed to occur on the adenylate cyclase level since (-)isoprenaline- or forskolin-stimulated activities behaved similarly and bacterial toxin-monitored Gs and Gi proteins remained stable. The mechanism of the initial decrease in hormonal responsiveness was further analysed in hybrid cells prepared by fusing reticulocytes with Friend erythroleukemia (MEL) cells. The hybrids contained reticulocyte-derived beta-adrenoceptors and MEL cell-derived adenylate cyclase and G proteins. Fusion of reticulocytes to native MEL cells caused adenylate cyclase activity to drop by 30% at 2 h and 45% at 18 h after fusion. By contrast, hybrids prepared after dimethylsulfoxide-induced differentiation of MEL cells showed stable or increasing rates of receptor-coupled cAMP formation between 2 and 18 h after fusion, concomitant with the enhanced activity of the Gs protein in these cells. A cyclase-stimulating factor present in the cytosol of MEL cells and of reticulocytes appeared not to be involved in short-term regulation of hormonal responsiveness. We conclude that the strength of beta-adrenergic responses in erythroid progenitor cells is primarily regulated by modulating G protein-mediated receptor cyclase coupling while reticulocytes, during early maturation, seem to rely on direct inactivation of adenylate cyclase, probably via a cytosolic proteolytic pathway.
Authors:
H Porzig; R Moudry; J B Montandon
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cellular physiology     Volume:  147     ISSN:  0021-9541     ISO Abbreviation:  J. Cell. Physiol.     Publication Date:  1991 Jun 
Date Detail:
Created Date:  1991-08-13     Completed Date:  1991-08-13     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0050222     Medline TA:  J Cell Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  439-46     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, University of Bern, Switzerland.
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MeSH Terms
Descriptor/Qualifier:
Adenylate Cyclase / metabolism
Animals
Catecholamines / pharmacology
Cell Differentiation / drug effects,  physiology
Cell Line
Cyclic AMP / metabolism
Erythroid Precursor Cells / cytology*,  metabolism,  physiology,  ultrastructure
Female
GTP-Binding Proteins / metabolism,  physiology
Hybrid Cells / cytology,  metabolism,  physiology,  ultrastructure
Leukemia, Erythroblastic, Acute / metabolism,  pathology,  physiopathology
Rats
Rats, Inbred Strains
Receptors, Adrenergic, beta / drug effects,  metabolism,  physiology*
Reticulocytes / cytology*,  metabolism,  physiology,  ultrastructure
Chemical
Reg. No./Substance:
0/Catecholamines; 0/Receptors, Adrenergic, beta; 60-92-4/Cyclic AMP; EC 3.6.1.-/GTP-Binding Proteins; EC 4.6.1.1/Adenylate Cyclase

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