1996 Fiscal Year Final Research Report Summary
Basic research in pathogenesis of BPH and phermaceutical therapy for BPH
| Project/Area Number |
07457367
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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 |
Urology
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| Research Institution | Gunma University |
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Principal Investigator |
YAMANAKA Hidetoshi Gunma university, School of medicine Pofessor, 医学部, 教授 (70110393)
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| Co-Investigator(Kenkyū-buntansha) |
FUKABORI Yoshitatsu Gunma university, School of medicine Assistant, 医学部, 助手 (90199167)
YUASA Hisako Gunma university, School of medicine Assistant, 医学部, 助手 (50240148)
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| Project Period (FY) |
1995 – 1996
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| Keywords | BPH / estrogen receptor / rat seminal vesicle / stromal cell / androgen receptor / pathogenesis |
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| Research Abstract |
On the basis of the working hypothesis that the essential pathogenesis of human benign prostatic hyperplasia might be the stromal proliferation, we are going to investigate how sex hormones and growth factors are involved in the stromal proliferation. We have already established the experimental model for stromal proliferation of male reproductive organs, that is, the stromal proliferation in the seminal vesicle after E2 injection to the immature castrated rats. We investigated the participation of estrogen in the stromal proliferation using this rat seminal vesicle model. On the other hand, in order to obtain the further understanding of the mechanism of stromal proliferation in human benign prostatic hyperplasia, we did the in vitro experiment using the cultured prostate stromal cells. We obtained the following results in 1996.
1) The experimental model : In 1995, we observed that the increase of ER (estrogen receptor) protein in the stromal cells concurred with the stromal proliferation. In 1996, we found that ER protein appeared in the basal cell as well as the stromal cell. Moreover, we found that the concomitant treatment of E2 with 5 alpha-DHT completely inhibited E2 mediated ER expression in both basal cell and stromal cell. This result suggests that ER works only when E2 is given in the absence of 5alpha-DHT.
2) The cultured prostate stromal cell : In 1995, Wwe observed that TGF-beta secretion from the cultured stromal cell increased in proportion to the decrease of DHT concentration in the culture-medium. In 1996, TGF-beta upregulated collagen production from the cultured stromal cell in the autocline fashion. Moreover, we found that this stromal cell had AR (androgen receptor) and expressed KGF in the presence of 5alpha-DHT.This result suggests that there exists DHT-AR-KGF system in this stromal cell.
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