| Project/Area Number |
05671366
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Osaka University |
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Principal Investigator |
HIROTA Kenji Osaka Univ.Med.School Lecturer, 医学部, 講師 (00189888)
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| Co-Investigator(Kenkyū-buntansha) |
KURACHI Hirohisa Osaka Univ.Med.School Assistant Professor, 医学部, 助手 (40153366)
小池 浩司 大阪大学, 医学部, 助手 (70225340)
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| Project Period (FY) |
1993 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1995: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1994: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1993: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | interleukin-6 / follicular stella cells / pituitary cells / pituitary adenylate cyclase activating polypeptide / vasoactive intestinal peptide / tyrosine kinase / 下垂体 / IL-6 / 下垂体濾胞状細胞 |
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| Research Abstract |
There is growing evidence that the neuro endocrine and immune systems are engaged in a functionally relevant crosstalk with each other. We and others reported that Interleukin-6 (IL-6) was produced by the normal anterior pituitary gland and that the source of IL-6 was folliculo-stellate (FS) cells, a pituitary cell type sharing many characteristics with cells of the immune system. In the pituitary gland. First we tested the effect of pituitary adenylate cydase activating polypeptide (PACAP) and vasoactive intestinal polypeptide (VIP) on IL-6 production by using recently established a pituitary FS-like cell line (TtT/GF). We found a significant increase of IL-6 production by PACAP and VIP with increase of intracellular cAMP concentrations. Next, we examined the effect of IL-6 on cell protiferation using the MtT/E rat pituiraty tumor cell line. Analysis of ^<125>I-rhIL-6 binding to the MtT/E cells indicated a dissociation constant of 0.953 X ^<10.9>M and the presence of 968 binding sites per cell. Incubation for 4 days with rhIL-6 caused dose-dependent stimulation of MtT/E cell growth. Addition of 20ng/ml IL-6 to the culture medium stimulated MtT/E cell growth in a time dependent manner. This effects was neutralized by the addition of anti-IL-6 antibody. In addition, stimulatory effect of IL-6 on MtT/E cell growth was inhibited by the tyrosine kinase inhibitor, suggesting that the possible involvement of thyrosine kinase in IL-6 signaling. Further we confirmed that FS cells stimulated basal PRL secretion by using co-culture system between TtT/GF cells and GH_3 cells. These findings provide further information to understand the physiological role of FS cell in the pituitary.
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