A2B receptor activation promotes glycogen synthesis in astrocytes through modulation of gene expression.

Détails

ID Serval
serval:BIB_CC56A622ABF8
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
A2B receptor activation promotes glycogen synthesis in astrocytes through modulation of gene expression.
Périodique
American Journal of Physiology. Cell Physiology
Auteur(s)
Allaman I., Lengacher S., Magistretti P.J., Pellerin L.
ISSN
0363-6143 (Print)
ISSN-L
0363-6143
Statut éditorial
Publié
Date de publication
03/2003
Peer-reviewed
Oui
Volume
284
Numéro
3
Pages
C696-C704
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
Adenosine has been proposed as a key factor regulating the metabolic balance between energy supply and demand in the central nervous system. Because astrocytes represent an important cellular element in the control of brain energy metabolism, we investigated whether adenosine could induce long-term changes of glycogen levels in primary cultures of mouse cortical astrocytes. We observed that adenosine increased glycogen content, up to 300%, in a time- (maximum at 8 h) and concentration-dependent manner with an EC(50) of 9.69 microM. Pharmacological experiments using the broad-spectrum agonist 5'-(N-ethylcarboxamido)adenosine (NECA) and specific agonists for the A(1), A(2A), and A(3) receptors [N(6)-cyclopentyladenosine (CPA), CGS-21680, and IB-MECA, respectively] suggest that the effect of adenosine is mediated through activation of the low-affinity A(2B) adenosine receptor subtype. Interestingly, adenosine induces in parallel the expression of the protein targeting to glycogen (PTG), one of the protein phosphatase-1 glycogen-targeting subunits that has been implicated in the control of glycogen levels in various tissues. These results indicate that adenosine can exert long-term control over glycogen levels in astrocytes and might therefore play a significant role in physiological and/or pathological processes involving long-term modulation of brain energy metabolism.
Mots-clé
Adenosine/agonists, Adenosine/antagonists & inhibitors, Animals, Animals, Newborn, Astrocytes/drug effects, Astrocytes/metabolism, CCAAT-Enhancer-Binding Proteins/drug effects, CCAAT-Enhancer-Binding Proteins/metabolism, Carrier Proteins/drug effects, Carrier Proteins/metabolism, Cells, Cultured, Central Nervous System/cytology, Central Nervous System/metabolism, Dose-Response Relationship, Drug, Energy Metabolism/drug effects, Energy Metabolism/physiology, Gene Expression Regulation/drug effects, Gene Expression Regulation/physiology, Glycogen/biosynthesis, Homeostasis/drug effects, Homeostasis/physiology, Intracellular Signaling Peptides and Proteins, Mice, Purinergic P1 Receptor Agonists, Purinergic P1 Receptor Antagonists, Receptor, Adenosine A2B, Receptors, Purinergic P1/metabolism
Pubmed
Web of science
Création de la notice
24/01/2008 14:17
Dernière modification de la notice
03/03/2018 21:28
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