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Titolo:
GROWTH HORMONE-RELEASING FACTOR REGULATION BY SOMATOSTATIN, GROWTH-HORMONE AND INSULIN-LIKE GROWTH-FACTOR-I IN FATAL RAT HYPOTHALAMIC-BRAINSTEM-CELL COCULTURES
Autore:
VAZQUEZ GF; CACICEDO L; DELOSFRAILES MT; LORENZO MJ; TOLON R; FRANCO FS;
Indirizzi:
CTR NACL INVEST CLIN,INST SALUD CARLOS III,SERV ENDOCRINOL E-28029 MADRID SPAIN HOSP RAMON Y CAJAL,SERV ENDOCRINOL MADRID SPAIN
Titolo Testata:
Neuroendocrinology
fascicolo: 6, volume: 58, anno: 1993,
pagine: 655 - 665
SICI:
0028-3835(1993)58:6<655:GHFRBS>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
HYPOPHYSEAL PORTAL BLOOD; ARCUATE NUCLEUS; FACTOR GRF; CONTAINING NEURONS; GH SECRETION; FACTOR IMMUNOREACTIVITY; (GH)-RELEASING FACTOR; FEEDBACK-REGULATION; NEGATIVE FEEDBACK; INVITRO RELEASE;
Keywords:
GRF; SS; GH; IGF-I; HYPOTHALAMIC-BRAIN STEM COCULTURES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
62
Recensione:
Indirizzi per estratti:
Citazione:
G.F. Vazquez et al., "GROWTH HORMONE-RELEASING FACTOR REGULATION BY SOMATOSTATIN, GROWTH-HORMONE AND INSULIN-LIKE GROWTH-FACTOR-I IN FATAL RAT HYPOTHALAMIC-BRAINSTEM-CELL COCULTURES", Neuroendocrinology, 58(6), 1993, pp. 655-665

Abstract

Information about growth hormone-releasing factor (GRF) regulation bysomatostatin, GH and IGF-I is scarce and controversial. This could bedue to the in vivo interactions among these signals and the lack of models for individualizing the action of one of them from the others upon GRF regulation. The aim of the present work was to study GRF regulation by these signals, using primary fetal rat hypothalamic-brain stemcell cocultures. Coculturing of these two cytotypes increases hypothalamic immunoreactive rat GRF (IR-rGRF) content in cells by 45% and in media by 36%. The effect of SS on GRF in cocultures was examined by using a multiple approach: (1) depleting endogenous SS by adding 1 mM cysteamine (CSH); (2) blocking endogenous SS by incubation with SS antiserum, and (3) incubating with synthetic SS14 at different concentrations and exposure periods. 1 mM CSH depleted IR-SS content (pg/plate, mean +/- SE) in cells (CSH-treated: 68 +/- 8 vs. control: 322 +/- 10, p<0.01) and media (CSH-treated: 211 +/- 15 vs. control: 880 +/- 70; p<O.O1). In the CSH-induced SS-depleted cultures, a slight reduction in the IR-rGRF content in cells was observed (CSH treated: 93.5 +/- 4.5 vs.control: 111 +/- 6; p<0.05), with no effect on media content. When SSantiserum was added to plates, there was a slight reduction in the IR-rGRF content in cells and media, but it was not significantly different from the controls. However, SS14 (10(-10) -10(-8) M) could not modify IR-rGRF content in media and cells. The GH effect on IR-rGRF was studied in the absence of CSH and in CSH-induced SS-depleted cultures. GH (5 mu M, 24 h) decreased (52%) the IR-rGRF content in media (GH-treated: 28.7 +/- 4.6 vs. control: 60.2 +/- 7; p<0.01) without causing changes in cell content. In SS-depleted cultures, the inhibitory action of GH on media IR-rGRF was greater (62% decrease) (GH-treated: not detected, control: 56 +/- 10; p<0.01) and also affected IR-rGRF cell content (GH-treated: 64.3 +/- 7.3 vs. control: 160 +/- 9.6; p<0.01). In thesame experiments, GH increased IR-SS content in cells (GH-treated: 31.8 +/- 4.6 vs. control 20.9 +/- 0.5; p<0.01) and in media (GH-treated:413 +/- 7 vs. control: 286 +/- 9; p<0.01). 1 mM CSH again depleted IR-SS content and abolished the GH stimulatory effect. IGF-I (5.6 nM, 24h) did not affect IR-rGRF content in media or in cells under either conditions (CSH and non-CSH-treated cultures). However, in these experiments IGF-I increased IR-SS content in the media (GH-treated: 322 +/- 3 vs. control: 289 +/- 9; p<0.05). These results indicate that: (1) Cocultures of brain stem and hypothalamic cells exert a positive action on the hypothalamic GRF; (2) locally secreted SS does not have an important role in the regulation of GRF in our experimental model; (3) GH has a direct inhibitory effect on GRF secretion which is independent of the SS released by GH; (4) IGF-I does not affect GRF at the concentration used in the experiment, and (5) CSH-treated fetal rat hypothalamic-brain stem cocultures provide information potentially useful in understanding GRF regulation independently from that of SS.

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Documento generato il 22/10/20 alle ore 15:23:38