2017 Fiscal Year Final Research Report
The mechanism of the development of benign prostatic hyperplasia via extra cellarer matrix.
Project/Area Number |
15K20102
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Urology
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Research Institution | Nagoya City University |
Principal Investigator |
Takashi Hamakawa 名古屋市立大学, 大学院医学研究科, 研究員 (40595394)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
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Keywords | 前立腺肥大症 / TSP-1 |
Outline of Final Research Achievements |
Previously, we reported that interleukin-18 (IL-18) may promote stromal hyperplasia in the prostate by inducing production of thrombospondin-1 (TSP-1) using BPH rat model. First, to clarify the role of TSP-1 in the development of BPH, we administered the IL-18-binding protein (IL-18BP), an inhibitor of IL-18, in the model rats. IL-18BP affected the dose-dependent decreases in TSP-1 mRNA expression levels. The collagen fibrils in the BPH tissues were likely decreased by IL-18BP. Next study, we aimed to determine the expression levels of TSP-1 in human prostate tissue and assess the correlation of these expressions and clinical parameters. Also, we investigated the correlation between the ratio of prostate biopsy tissue component and IL-18 and TSP-1 expression. As a result, TSP-1 was positively correlated with prostate volume. A positive correlation was found between IL-18 expression and the ratio of glandular epithelium, and between TSP-1 expression and the area of smooth muscle.
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Free Research Field |
前立腺肥大症
|