| Project/Area Number |
09470353
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Gunma University |
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Principal Investigator |
MINEGISHI Takashi Gunma University School of Medicine, Dept.of OB/GYN,Assistant Professor, 医学部, 講師 (00209842)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1998: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | Gonadotropin Receptor / Activin / FSH / IGF-I / PRL / mRNA / FSHレセプター / LHレセプター / ルシフェラーゼ活性 / ラット顆粒膜細胞 / cAMP |
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| Research Abstract |
FSH is required to maintain FSH and LH receptor at elevated steady state levels after receptor induction in the granulosa cells of diesthystillbesterol (DES)-primed immature rats. To identify the mechanisms underlying the hormone-dependent induction and maintenance of LH receptor (LH-R) in rat granulosa cells, the effect of FSH and some local factors on the LH-R mRNA levels were studied. In order to study the transcriptional regulation of the LH-R, we have isolated a 5' -flanking region of the rat LH-R gene and subcloned nucleotide -1 (relative to the translational initiation codon) to -1379 into a luciferase reporter plasmid. Treatment with 8-Br-cAMP and ESH significantly enhanced activity of 1379 bp of LH-R 5' -flanking region in a dose dependent manner. This data clearly demonstrates that FSH (mediated by CAMP) stimulates the induction of the LH-R in granulosa cells of DES-primed immature rats, at least in part, through increasing the rate of transcription of the LH-R gene. in the presence of FSH, IGF-1 augments FSH receptor mRNA.These results show that IGF-1 is one of the important factors that act in the medium to maintain LH-R levels in granulosa cells.
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