Insulin-Like Growth Factor-1 Stimulated DNA Replication in Mouse Endometrial Stromal Cells

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  • INOUE Ayako
    Department of Biology, Faculty of Science, Okayama University
  • TAKEUCHI Sakae
    Department of Biology, Faculty of Science, Okayama University
  • TAKAHASHI Sumio
    Department of Biology, Faculty of Science, Okayama University

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  • Insulin-Like Growth Factor-I Stimulated DNA Replication in Mouse Endometrial Stromal Cells

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Much evidence has suggested that sex steroid hormone-induced growth of uterine cells is mediated by polypeptide growth factors synthesized in uterine tissues. The present study aimed to clarify the effect of insulin-like growth factor-I (IGF-I) on the proliferation of mouse endometrial stromal cells obtained from immature mice. IGF-I and IGF-I receptor (type I) mRNAs were detected in the endometrial stromal cells. IGF-I increased bromodeoxyuridine (BrdU) uptake in the endometrial stromal cells, indicating an increase in DNA replication. E2 increased IGF-I mRNA levels in the endometrial stromal cells. IGF-I receptor is a tyrosine kinase receptor, and treatment with genistein, a tyrosine kinase inhibitor, reduced IGF-I-induced BrdU-uptake in the endometrial stromal cells. IGF-I signaling pathways involve mitogen-activated protein (MAP) kinase and phosphatidylinositol-3 kinase (PI-3 kinase). Treatment with 10-7 M of the MAP kinase inhibitor PD098059 and 10-5 M of the PI-3 kinase inhibitor LY294002 decreased IGF-I-induced BrdU-uptake in the endometrial stromal cells. However, LY294002 (10-5 M) also decreased the BrdU-uptake in the absence of IGF-I treatment. These results suggest that endometrial IGF-I is involved in the proliferation of endometrial stromal cells in a paracrine or autocrine manner, and that the MAP kinase pathway is involved in DNA replication of endometrial stromal cells.<br>

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