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Titolo:
GNRH SIGNALING PATHWAYS AND GNRH-INDUCED HOMOLOGOUS DESENSITIZATION IN A GONADOTROPE CELL-LINE (ALPHA-T3-1)
Autore:
POULIN B; RICH N; MAS JL; KORDON C; ENJALBERT A; DROUVA SV;
Indirizzi:
CTR PAUL BROCA,U159 INSERM,UNITE DYNAM SYST NEUROENDOCRINIENS,2 RUE DALESIA F-75014 PARIS FRANCE CTR PAUL BROCA,U159 INSERM,UNITE DYNAM SYST NEUROENDOCRINIENS F-75014PARIS FRANCE UNIV MEDITERRANEE,ICNE,UMR 6544 CNRS,FAC MED F-13916 MARSEILLE 20 FRANCE
Titolo Testata:
Molecular and cellular endocrinology
fascicolo: 1-2, volume: 142, anno: 1998,
pagine: 99 - 117
SICI:
0303-7207(1998)142:1-2<99:GSPAGH>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-C; THYROTROPIN-RELEASING-HORMONE; CYTOSOLIC PHOSPHOLIPASE A(2); MESSENGER-RNA LEVELS; PITUITARY-CELLS; ARACHIDONIC-ACID; DOWN-REGULATION; LUTEINIZING-HORMONE; RAPID DESENSITIZATION; COUPLED RECEPTORS;
Keywords:
ALPHA-T3-1 CELLS; GONADOTROPE CELL LINE; GNRH; PHOSPHOLIPASE-C; PHOSPHOLIPASE-A(2); PHOSPHOLIPASE-D; PROTEIN KINASE-C ISOENZYMES; G PROTEINS; ARACHIDONIC ACID; INOSITOL PHOSPHATES; HOMOLOGOUS DESENSITIZATION; DOWN-REGULATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
65
Recensione:
Indirizzi per estratti:
Citazione:
B. Poulin et al., "GNRH SIGNALING PATHWAYS AND GNRH-INDUCED HOMOLOGOUS DESENSITIZATION IN A GONADOTROPE CELL-LINE (ALPHA-T3-1)", Molecular and cellular endocrinology, 142(1-2), 1998, pp. 99-117

Abstract

Exposure of the gonadotrope cells to gonadotropin-releasing hormone (GnRH) reduces their responsiveness to a new GnRH stimulation (homologous desensitization). The time frame as well as the mechanisms underlying this phenomenon are yet unclear. We studied in a gonadotrope cell line (alpha T3-1) the effects of short as well as long term GnRH pretreatments on the GnRH-induced phospholipases-C (PLC), -A(2) (PLA(2)) and-D (PLD) activities, by measuring the production of IP3, total inositol phosphates (IPs), arachidonic acid (AA) and phosphatidylethanol (PEt) respectively. We demonstrated that although rapid desensitization of GnRH-induced IF, formation did not occur in these cells, persistent stimulation of cells with GnRH or its analogue resulted in a time-dependent attenuation of GnRH-elicited IPs formation. GnRH-induced IPs desensitization was potentiated after direct activation of PKC by the phorbol ester TPA, suggesting the involvement of distinct mechanisms in the uncoupling exerted by either GnRH or TPA on GnRH-stimulated PI hydrolysis. The levels of individual phosphoinositides remained unchanged under any desensitization condition applied. Interestingly, while the GnRH-induced PLA(2) activity was rapidly desensitized (2.5 min) after GnRH pretreatments, the neuropeptide-evoked PLD activation was affected at later times, indicating an important time-dependent contribution of these enzymatic activities in the sequential events underlying the GnRH-induced homologous desensitization processes in the gonadotropes. Under GnRH desensitization conditions, TPA was still able to induce PLD activation and to further potentiate the GnRH-evoked PLD activity. alpha T3-1 cells possess several PKC isoforms which, except PKC zeta, were differentially down-regulated by TPA (PKC alpha, beta(II), delta,epsilon, eta) or GnRH (PKC beta(II), delta, epsilon, eta). In spite of the presence of PKC inhibitors or down-regulation of PKC isoforms byTPA, the desensitizing effect of the neuropeptide on GnRH-induced IPs, AB and PEt formation remained unchanged. In conclusion, in alpha T3-1 cells the GnRH-induced homologous desensitization affects the GnRH coupling with PLC, PLA, and PLD by mechanism(s) which do not implicate TPA-sensitive PKC isoforms, but likely reflect time-dependent modification(s) on the activation processes of the enzymes. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.

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Documento generato il 04/04/20 alle ore 14:25:55