2002 Fiscal Year Final Research Report Summary
Mechanism of prolactin action on induction of development, enlargement and inflammation of prostate -study with prolactin knockout mice-
| Project/Area Number |
13670136
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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 |
Pathological medical chemistry
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| Research Institution | Nippon Veterinary and Animal Science University (2002)
Mie University (2001) |
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Principal Investigator |
TANAKA Minoru Nippon Veterinary and Animal Science University, Department of Nippon Veterinary and Animal Science University, Professor, 獣医畜産学部, 教授 (90024736)
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| Co-Investigator(Kenkyū-buntansha) |
OHTA Yoshiyuki Nippon Veterinary and Animal Science University, Department of Nippon Veterinary and Animal Science University, Lecturer, 獣医畜産学部, 講師 (00277667)
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| Project Period (FY) |
2001 – 2002
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| Keywords | prolactin / prostate / inflammation / knockout mouse / prolactin receptor / gene expression / bisphenol A |
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| Research Abstract |
It is suggested that chronic hyperprolactinemia in infant mice induced by estrogen causes inflammation in the prostate. To prove the prolactin action on the prostate, extents of inflammation in wild-type and prolactin-knockout (PRL-KO) mice were examined after administration of an estrogenic compound, bisphenol A. The myeloperoxidase activity in the wild-type mice was increased by the treatment, but the activity remained at basal level in PRL-KO mice. These results indicate mat the inflammation ** the prostate is mediated by PRL. In order to clarify the molecular mechanisms of PRL action on the prostate, PRL-receptor (PRL-R) gene expression was analyzed. In addition of the known three first exons, El-1, El-2 and El-3, two novel first exons, El-4 and El-5, were identified in rat PRL-R gene. Each first exon is expressed in a tissue-specific manner. RT-PCR analysis repealed the expression of El-3 exon in the prostate. It has been known that the expression of El-3 was regulated by SP-1 and C/EBPβ, suggesting that the expression of PRL-R gene in the prostate is regulated by these two transcription factors.
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