Regulation of cell proliferation and spontaneous contraction through a KIT-mediated mechanism in benign prostatic hyperplasia
| Project/Area Number |
24791659
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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 |
IMURA Makoto 名古屋市立大学, 医学(系)研究科(研究院), 研究員 (00551269)
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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: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | KIT陽性細胞 / 前立腺肥大症 |
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| Outline of Final Research Achievements |
KIT-positive interstitial cells in the gut are considered to function as a growth factor of stroma. Several reports have shown the existence of KIT-positive interstitial cells in the prostate. However, the role of these cells in the prostate has remained unclear. In this study, we examined the function of KIT-positive interstitial cells in BPH.
KIT was localized in interstitial cells of the stromal component in human prostate and guinea pig prostate. SCF administration increased cell proliferation dose-dependently for human prostate stromal cell line (PrSC). Treatment with SCF increased the expression of JAK2 and STAT1 dose-dependently in PrSCs. KIT expression in BPH were found to be significantly larger than in normal human prostate. Imatinib administration inhibited spontaneous contractions of guinea pig prostate dose-dependently.The role of KIT and KIT-positive cells in prostate may be related to the regulation of cell proliferation and spontaneous contraction.
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Report
(4 results)
Research Products
(6 results)
