| Project/Area Number |
18591784
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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 | Kyoto Prefectural University of Medicine |
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Principal Investigator |
SOH Jintetsu Kyoto Prefectural University of Medicine, Graduate School of Medicine, Assistant Professor (40305587)
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| Co-Investigator(Kenkyū-buntansha) |
NAITOH Yasuyuki Kyoto Prefectural University of Medicine, Graduate School of Medicine, Assistant Professor (50405312)
NAKAMURA Terukazu Kyoto Prefectural University of Medicine, Graduate School of Medicine, Assistant Professor (10381964)
MIZUTANI Yoichi Kyoto Prefectural University of Medicine, Graduate School of Medicine, Associate professor (10243031)
KAWAUCHI Akihiro Kyoto Prefectural University of Medicine, Graduate School of Medicine, Associate professor (90240952)
MIKI Tsuneharu Kyoto Prefectural University of Medicine, Graduate School of Medicine, professor (10243239)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,860,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥360,000)
Fiscal Year 2007: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2006: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | erectile dysfunction / diabetes mellitus / human cavernous smooth muscle cell / tisuue regeneration |
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| Research Abstract |
Diabetes mellitus is the most prevalent cause of sexual dysfunction including erectile and ejaculation difficulties. It has been reported that 20-85% of men with diabetes complain of erectile dysfunction (ED). In fact, diabetic patients have a risk of developing ED approximately three times higher than non- diabetic subjects. While the involvement of neurovascular factors in erectile function has been documented in experimental animals, the molecular mechanisms underlying ED in diabetic patients still remain to be. clarified. To elucidate the possible elements involved in ED in diabetes mellitus, we examined streptozotocin (STZ)-induced diabetic rats.
Adult male Wistar rats (10-weeks old) were randomized into two groups. One group received a single intraperitoneal injection of 60 mg/kg STZ dissolved in citrate phosphate buffer. The control rats in the other group were injected with an equal volume of citrate buffer. We carried out a broad-scale gene expression profiling using cDNA array
… More
in the penises of the STZ-induced diabetic rats. The total RNA isolated at 2, 4, 8 and 12 weeks after STZ injections was subjected to Northern blot analyses and localization of IGFBP-3 in the rat penises. Immunohistochemical staining was performed. Morphometric analyses of the smooth muscle and connective tissue in the diabetic rat penises were performed with Azan. Intracavernous pressure was measured following electrostimulation.
Among the genes investigated, the expression level of insulin-like growth factor binding protein 3 (IGFBP-3) had increased markedly at 12 weeks after the STZ treatment. Increased levels of IGFBP-3 mRNA were demonstrated at as early as 2 weeks after induction of hyperglycemia. Increased IGFBP-3 protein was localized to the epithelium of the urethra, the penile endothelium, and to the smooth muscle in the corpus cavernosum. Significant depletion of the smooth muscle density relative to the connective tissue was first observed in the penises of the 8 week-diabetic rats, whereas a significant reduction in the intracavernous pressure was demonstrated only at 12 weeks after induction of hyperglycemia.
We demonstrated increased expression of IGFBP-3 in the penile endothelium and the smooth muscle of the corpus cavernosum in the diabetic rat. The present findings suggest that increased expression of IGFBP-3 is not a result of ED, but possibly plays an important role in its development. Less
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