Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 1 de 1
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
1.
J Neuroendocrinol ; 28(4)2016 04.
Artigo em Inglês | MEDLINE | ID: mdl-26670189

RESUMO

Oxytocin secretion is required for successful reproduction. Oxytocin is synthesised by magnocellular neurones of the hypothalamic supraoptic and paraventricular nuclei and the physiological demand for oxytocin synthesis and secretion is increased for birth and lactation. Therefore, we used a polymerase chain reaction (PCR) array screen to determine whether genes that might be important for synthesis and/or secretion of oxytocin are up- or down-regulated in the supraoptic and paraventricular nuclei of late-pregnant and lactating rats, compared to virgin rats. We then validated the genes that were most highly regulated using real time-quantitative PCR. Among the most highly regulated genes were those that encode for suppressors of cytokine signalling, which are intracellular inhibitors of prolactin signalling. Prolactin receptor activation changes gene expression via phosphorylation of signal transducer and activator of transcription 5 (STAT5). Using double-label immunohistochemistry, we found that phosphorylated STAT5 was expressed in almost all oxytocin neurones of late-pregnant and lactating rats but was almost absent from oxytocin neurones of virgin rats. We conclude that increased prolactin activation of oxytocin neurones might contribute to the changes in gene expression by oxytocin neurones required for normal birth and lactation.


Assuntos
Regulação da Expressão Gênica , Núcleo Hipotalâmico Paraventricular/metabolismo , Reprodução/genética , Fator de Transcrição STAT5/biossíntese , Núcleo Supraóptico/metabolismo , Animais , Feminino , Lactação/metabolismo , Neurônios/metabolismo , Ocitocina/genética , Fosforilação , Gravidez , Ratos , Fator de Transcrição STAT5/genética , Fator de Transcrição STAT5/metabolismo
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...