| Project/Area Number |
13670058
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Environmental physiology (including Physical medicine and Nutritional physiology)
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| Research Institution | University of Yamanashi (Faculty of Medicine) |
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Principal Investigator |
ARITA Jun University of Yamanashi, Faculty of Medicine, Professor, 医学部, 教授 (80128587)
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| Co-Investigator(Kenkyū-buntansha) |
KAWASHIMA Kengo University of Yamanashi, Faculty of Medicine, Research Associate, 医学部, 助手 (70324184)
YAMAKAWA Koji University of Yamanashi, Faculty of Medicine, Research Associate, 医学部, 助手 (90293472)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2002: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2001: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Estrogen / Cell Proliferation / Prolactin / Anterior Pituitary Gland / Insulin / Growth Factor |
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| Research Abstract |
Studies using rat lactotrophs in primary culture in 2001
1 Estradiol (E2) stimulated basal proliferation of lactotrophs in primary culture with a long latency, 96 h, while it inhibited insulin-induced proliferation within 12 h. The ED50 were 8 and 85 pM for the E2 mitogenic and antimitogenic actions, respectively.
2 This antimitogenic action was dependent upon the estrogen activity and not observed for androgens and progestins.
3 In addition to the mitogenic action, the E2 antimitogenic action was antagonized by antiestrogens, indicating an estrogen receptor-mediated action.
4 E2 inhibited not only insulin-induced lactotroph proliferation but also insulin-like growth factor-1 (IGF-1)-induced proliferation while it enhanced proliferation induced by serum or increased levels of intracellular cyclic AMP, suggesting that the E2 antimitogenic action is not dependent upon proliferative levels but mitogen-specific.
Studies using prolactin-producing cell lines in 2002
1 In GH_3 cells, E2 inhibited IGF-1-induced proliferation and stimulated serum-induced proliferation as in lactotrophs in primary culture. However, E2 failed to stimulate basal proliferation of GH_3 cells.
2 In another prolactin-producing cell line, GH_4C_1 cells, E2 inhibited IGF-1-induced proliferation and, unlike to GH_3 cells, stimulated basal proliferation.
3 Double immunostaining for prolactin and the cell cycle-regulating protein cyclin D1 revealed that stimulation and inhibition of lactotroph proliferation induced by the mitogenic and antimitogenic actions of E2, respectively, were associated with parallel changes in the number of cyclin D1-immunoreactive lactotrophs.
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