1996 Fiscal Year Final Research Report Summary
REGULATION OF PROSTATIC GROWTH AND FUNCTION BY EPITHELIAL-STROMAL INTERACTION AND TESTICULAR FACTOR.
| Project/Area Number |
06671576
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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 |
Urology
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| Research Institution | TOKYO MEDICAL AND DENTAL UNIVERSITY |
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Principal Investigator |
ISHIZAKA Kazuhiro TOKYO MEDICAL AND DENTAL UNIVERSITY,SCH OF MED,STUFF UROLOGIST, 医学部, 助手 (60168218)
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| Co-Investigator(Kenkyū-buntansha) |
KITAHARA Satoshi TOKYO MEDICAL AND DENTAL UNIVERSITY,SCH OF MED,ASSISTANT PROFESSOR, 医学部, 講師 (10186257)
KIHARA Kazunori TOKYO MEDICAL AND DENTAL UNIVERSITY,SCH OF MED,ASSISTANT PROFESSOR, 医学部, 講師 (40161541)
AZUMA Hiroshi TOKYO MEDICAL AND DENTAL UNIVERSITY,MEDICAL CHEMISTRY,FACULTY OF MEDICINE AND IN, 医用機材研究所, 助教授 (20134736)
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| Project Period (FY) |
1994 – 1996
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| Keywords | PROSTATE / ANDROGEN / INSULIN-LIKE GROWTH FACTOR (IGF) / ENDOTHELIN |
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| Research Abstract |
Canine prostatic epithelial cells and stromal cells in primary culture were subjected to growth assay by comparing cell density of each well. Dihydrotestosterome increased epithelial cell growth.
Addition of stromal cell-conditioned medium increased epithelial cell growth, biphasically. The effect was reversed to control levels by adding anti-rat Insulin-like growth factor II (IGF-II) antibody. Reccombinant human IGF-II stimulated epithelial cell growth biphasically. Immunochemical dot blot and Northern blot demonstrated the presence of an IGF-II-like substance in stromal cell-conditioned medium and the stromal cell lysate and IGF-II mRNA expression in cultured stromal cells, respectively. Therefore, it appears most likely that canine prostatic stromal cells produce and secrete IGF-II-like substance which stimulates canine prostatic epithelial cell growth.
Endothelin (ET)-1 or ET-3 increased epithelial cell density. The effect of ET-1 was reversed by ETB antagonist but not by ETA antagonist. Immuno-reactive ET-1-like substance was detected in epithelial cell-conditioned medium by radioimmunoassay. ET-1 binding sites was localized within the glandular epithelium, which was blocked by ETB andtagonist but not by ETA antagonist. Therefore, it appears likely that ETs stimulate canine prostatic epithelial cell growth via ETB receptors.
In connclusion, growth of canine prostatic epithelial cell seems to be regulated by endocrine, paracrine and autocrine pathways. The relation and regulation of those pathways will be studied in future.
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