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Titolo:
Cortisol suppresses prolactin release through a non-genomic mechanism involving interactions with the plasma membrane
Autore:
Borski, RJ; Hyde, GN; Fruchtman, S; Tsai, WS;
Indirizzi:
N Carolina State Univ, Dept Zool, Raleigh, NC 27695 USA N Carolina State Univ Raleigh NC USA 27695 pt Zool, Raleigh, NC 27695 USA
Titolo Testata:
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY B-BIOCHEMISTRY & MOLECULAR BIOLOGY
fascicolo: 2-3, volume: 129, anno: 2001,
pagine: 533 - 541
SICI:
1096-4959(200106)129:2-3<533:CSPRTA>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
TILAPIA OREOCHROMIS-MOSSAMBICUS; MAMMARY-TUMOR VIRUS; OSMOTIC-PRESSURE; PITUITARY-GLAND; BINDING-PROTEIN; GENE-EXPRESSION; TELEOST FISH; RECEPTOR; INVITRO; CELL;
Keywords:
BSA-conjugated steroid; osmoregulation; pituitary; receptors; calcium; cAMP; cycloheximide; tilapia; hydrocortisone; glucocorticoid;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Borski, RJ N Carolina State Univ, Dept Zool, Box 7617, Raleigh, NC 27695 USA N Carolina State Univ Box 7617 Raleigh NC USA 27695 C 27695 USA
Citazione:
R.J. Borski et al., "Cortisol suppresses prolactin release through a non-genomic mechanism involving interactions with the plasma membrane", COMP BIOC B, 129(2-3), 2001, pp. 533-541

Abstract

In the classical theory of steroid hormone action, steroids diffuse through the membrane and alter transcription of specific genes resulting in synthesis of proteins important for modulating cell function. Most often, steroids work solely through the genome to exert their physiological actions in aprocess that normally takes hours or days to occur. In tilapia (Oreochromis mossambicus), cortisol inhibits prolactin (PRL) release within 10-20 min in vitro. This action is accompanied by similarly rapid reductions in cellular Ca2+ and cAMP levels, second messengers known to transduce the membraneeffects of peptide hormones. We further examined whether cortisol might inhibit PRL release through a non-genomic, membrane-associated mechanism using the protein synthesis inhibitor, cycloheximide, and a membrane impermeantform of cortisol, cortisol-21 hemisuccinate BSA (HEF/BSA). Cycloheximide (2 and 10 mug/ml) was ineffective in overcoming PRL release induced by hyposmotic medium or that inhibited by cortisol over 4 h static incubations. These dosages reduced protein synthesis as measured by amino acid incorporation in pituitaries by 75 and 99%, respectively. During 4-h incubation, HEF/BSA and HEF significantly reduced PRL release in a dose-dependent fashion. These studies suggest that cortisol inhibits PRL release through a plasma membrane-associated, protein-synthesis independent (non-genomic) pathway. (C) 2001 Elsevier Science Inc. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 16:16:14