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Titolo:
Ontogeny of corticosterone-inducible growth hormone-secreting cells duringchick embryonic development
Autore:
Bossis, I; Porter, TE;
Indirizzi:
Univ Maryland, Dept Anim & Avian Sci, College Pk, MD 20742 USA Univ Maryland College Pk MD USA 20742 Avian Sci, College Pk, MD 20742 USA
Titolo Testata:
ENDOCRINOLOGY
fascicolo: 7, volume: 141, anno: 2000,
pagine: 2683 - 2690
SICI:
0013-7227(200007)141:7<2683:OOCGHC>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
RIBONUCLEIC-ACID EXPRESSION; GH-RELEASING HORMONE; GLUCOCORTICOID RECEPTOR; PITUITARY-GLAND; GENE-EXPRESSION; ANTERIOR-PITUITARY; SOMATOTROPH DIFFERENTIATION; RETINA DEVELOPMENT; BINDING-SITES; FETAL RATS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
59
Recensione:
Indirizzi per estratti:
Indirizzo: Porter, TE Univ Maryland, Dept Anim & Avian Sci, College Pk, MD 20742 USA Univ Maryland College Pk MD USA 20742 College Pk, MD 20742 USA
Citazione:
I. Bossis e T.E. Porter, "Ontogeny of corticosterone-inducible growth hormone-secreting cells duringchick embryonic development", ENDOCRINOL, 141(7), 2000, pp. 2683-2690

Abstract

We reported that corticosterone administration into the albumen of fertilechicken eggs on embryonic day (e) 11 induces an increase in the populationof GH-secreting cells. The present study evaluated the ontogeny, dose response, localization, and persistence of the glucocorticoid-induced increase in the somatotroph population during chicken embryonic development. Corticosterone (0, 0.02, 0.2, and 2 mu g in 300 mu l saline) was injected into separate eggs on e9, e10, e11 and e12, and the population of GH-secreting cells was assessed 2 days later using reverse hemolytic plaque assays. Corticosterone treatment on e9 or e10 was unable to increase the population of GH-secreting cells on e11 or e12. In contrast, 0.2 and 2 mu g of corticosteroneon ell increased the population of GH-secreting cells on e13 (P < 0.05, n = 3 experiments) to 8.2 +/- 0.6 and 6.4 +/- 0.5% of all cells, respectively, relative to controls (2.4 +/- 0.2%). For e14 embryos heated on e12, only the 2 mu g dose increased the proportion of GH-secreting cells (6.4 +/- 0.6%) relative to controls (3.6 +/- 0.4%). In a second experiment, 0, 0.02, 0.2, 2, and 20 mu g of corticosterone were injected on e0, e8, e9, e10, e11, and e12, and the population of GH-secreting cells was assessed on e13 in all groups. No dose of corticosterone was effective when given on e0, e8, e9,or e10. The 0.2 mu g and 2 mu g doses increased the population of GH-secreting cells (7.6 +/- 0.9% and 6.7 +/- 0.8%, respectively) relative to controls (2.3 +/- 0.4%) when injected on e11 (P < 0.05, n = 4 experiments). The 2-mu g dose also increased GH cell abundance when injected on e12 (5.6 +/- 0.4%), relative to controls (2.7 +/- 0.5%). Treatment with 20 mu g on e11 and e12 induced the greatest responses (10.3 +/- 1.1% and 8.7 +/- 0.9%, respectively). However, in subsequent experiments, administration of 20 mu g on e11 resulted in embryonic death by e18. In a third set of experiments, two groups of eggs were injected either with 2 mu g of corticosterone in salineor saline alone on e11, and the number of GH-secreting cells was estimatedon e13, e16, e19, and the day of hatch (d1). The population of GH-secreting cells in corticosterone treated embryos was significantly higher than in saline treated embryos only on e13 (7.1 +/- 0.8% and 2.7 +/- 0.3%, respectively). No significant differences were observed on e16 (12.4 +/- 1.5% and 13.6 +/- 1.2%), e19 (19.0 +/- 1.0% and 18.2 +/- 1.7%) and d1 (23.8 +/- 2.1% and 25.1 +/- 1.8%) between corticosterone treated and control embryos, respectively. In a fourth set of experiments, whole mount in situ hybridizationindicated that injection of corticosterone on ell induced GH messenger RNAexpression in the caudal part of the pituitary gland on e13, where somatotrophs are located normally later in development. We conclude that corticosterone administration in ovo can increase the population of GH-secreting cells in the caudal anterior pituitary only during a small window of development between ell and e13 and that this premature increase of GH-secreting cells does not affect the percentage of GH-secreting cells later in development.

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Documento generato il 25/11/20 alle ore 04:19:01