The mechanism of the development of benign prostatic hyperplasia via pro-inflammatory cytokine IL-18.
| Project/Area Number |
24791665
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Urology
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| Research Institution | Nagoya City University |
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Principal Investigator |
HAMAKAWA Takashi 名古屋市立大学, 医学(系)研究科(研究院), 臨床研究医 (40595394)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 前立腺肥大症 / 炎症 / IL-18 / TSP-1 |
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| Outline of Final Research Achievements |
Inflammation may plays an important role in the development of benign prostatic hyperplasia (BPH). Previously, we used a stromal hyperplasia rat model and analyzed the genomic profile of this model by using cDNA microarray. We focused on the most expressed pro-inflammatory cytokine IL-18 in several cytokine genes related to the inflammatory response.
IL-18 was localized in the epithelial and stromal components in rat and human BPH tissues. IL-18 receptor was strongly localized in smooth muscle cells both normal prostate tissues and BPH tissues. In human cultured prostate smooth muscle cells, IL-18 effected dose-dependent increases in the TSP-1 levels. TSP-1 promoted proliferation of human cultured prostate stromal cells. Our findings suggest IL-18 in which secreted in epithelial cells, stimulates TSP-1 production by smooth muscle cells. TSP-1 then promotes the proliferation of prostatic stromal cells, which in turn leads to the development of prostatic hyperplasia.
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Report
(4 results)
Research Products
(7 results)
