Antagonic effects of oestradiol in interaction with IGF-1 on proliferation of lactotroph cells in vitro
Autor: | Silvina Gutiérrez, Agustín Aoki, Elsa Margarita Orgnero, Jorge Humberto Mukdsi, Alicia Inés Torres, Juan Pablo Petiti, Ana Lucía De Paul |
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Rok vydání: | 2005 |
Předmět: |
MAPK/ERK pathway
endocrine system medicine.medical_specialty Histology Protein Kinase C-alpha Genistein Protein Kinase C-epsilon Receptor tyrosine kinase Prolactin cell chemistry.chemical_compound Western blot Pituitary Gland Anterior Internal medicine medicine Animals Insulin-Like Growth Factor I Phosphorylation Rats Wistar Extracellular Signal-Regulated MAP Kinases Molecular Biology Protein kinase C Cells Cultured Cell Proliferation medicine.diagnostic_test biology Estradiol Cell growth Cell Biology Rats Medical Laboratory Technology Endocrinology chemistry Cell culture biology.protein Female |
Zdroj: | Histochemistry and cell biology. 124(3-4) |
ISSN: | 0948-6143 |
Popis: | The effects of IGF-1, 17 beta oestradiol and its functional interaction on lactotrophs cell proliferation were evaluated. In addition we investigated the involvement of PKC alpha, epsilon and phosphorilated ERK, in the mitogenic process. Primary cell cultures of adenohypophysis from female Wistar rats were studied in serum free conditions. The proliferation of lactotrophs was determined by double immunostaining for BrdU and PRL. The incubation with IGF-1 5, 30 or 100 ng/ml during 48 or 72 h increased lactotrophs proliferation two-threefold depending on IGF-1 concentration. Co-incubation of IGF-1 (30 ng/ml) with genistein (25 microM) or BIM (0.5 or 2 microM), lowered of tyrosine kinase receptor or of PKC respectively, inhibited the induced IGF-1 lactotrophs proliferation. 17 beta oestradiol (1, 10 or 100 nM) had not mitogenic effect, whereas in the presence of serum PRL cells proliferation was stimulated. Co-incubation with 1 nM oestradiol and IGF-1 significantly decreased the lactotroph BrdU-labelling achieved with IGF-1. PKC alpha, epsilon and ERK1/2 levels measured by western blot augmented in the presence of IGF-1 and were inhibited with the addition of genistein, supporting a participation of these enzymes in the proliferate process. Co-incubation of IGF-1 with 1 nM oestradiol decreased both PKC isoforms and activated ERK1/2 levels, suggesting that oestradiol would exert its antiproliferative effect by acting on the signalling pathway of IGF-1. The results revealed antagonic effects of oestradiol on lactotroph proliferation depending on its concentration and the presence of IGF-1. |
Databáze: | OpenAIRE |
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