Regulation and glucocorticoid-independent induction of lipocortin I in cultured astrocytes.

Détails

ID Serval
serval:BIB_A66C84C31FF6
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Regulation and glucocorticoid-independent induction of lipocortin I in cultured astrocytes.
Périodique
Journal of Neurochemistry
Auteur⸱e⸱s
Gebicke-Haerter P.J., Schobert A., Dieter P., Honegger P., Hertting G.
ISSN
0022-3042 (Print)
ISSN-L
0022-3042
Statut éditorial
Publié
Date de publication
1991
Volume
57
Numéro
1
Pages
175-183
Langue
anglais
Résumé
Stimulation of prostaglandin (PG) release in rat astroglial cultures by various substances, including phorbol esters, melittin, or extracellular ATP, has been reported recently. It is shown here that glucocorticoids (GCs) reduced both basal and stimulated PGD2 release. Hydrocortisone, however, did not inhibit ATP-, calcium ionophore A23187-, or tetradecanoyl phorbol acetate (TPA)-stimulated arachidonic acid release, and only TPA stimulations were affected by dexamethasone. GC-mediated inhibition of PGD2 release thus appeared to exclude regulation at the phospholipase A2 (PLA2) level. Therefore, the effects of GCs on the synthesis of lipocortin I (LC I), a potent, physiological inhibitor of PLA2, were studied in more detail. Dexamethasone was not able to enhance de novo synthesis of LC I in freshly seeded cultures and failed to increase LC I synthesis in 2-3-week-old cultures. It is surprising that LC I was the major LC synthesized in those cultures, and marked amounts accumulated with culture time, reaching plateau levels at approximately day 10. In contrast, LC I was barely detectable in vivo. This tonic inhibition of PLA2 is the most likely explanation for unsuccessful attempts to evoke PG release in astrocyte cultures by various physiological stimuli. GC receptor antagonists (progesterone and RU 38486) given throughout culture time reduced LC I accumulation and simultaneously increased PGD2 release. Nonetheless, a substantial production of LC I persisted in the presence of antagonists. Therefore, LC I induction did not seem to involve GC receptor activation. This was confirmed in serum- and GC-free brain cell aggregate cultures. Here also a marked accumulation of LC I was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
Mots-clé
Animals, Annexins, Astrocytes/metabolism, Brain/cytology, Brain/metabolism, Calcium-Binding Proteins/metabolism, Cell Aggregation, Cells, Cultured, Glucocorticoids/pharmacology, Phospholipases/antagonists & inhibitors, Prostaglandin D2/antagonists & inhibitors, Receptors, Glucocorticoid/antagonists & inhibitors, Time Factors, Up-Regulation
Pubmed
Web of science
Création de la notice
24/01/2008 13:11
Dernière modification de la notice
20/08/2019 15:11
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