2007 Fiscal Year Final Research Report Summary
Research for erectile dysfunction by DNA microarray assay and PWV/PVM
| Project/Area Number |
18591781
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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 | The University of Tokyo |
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Principal Investigator |
NISHIMATSU Hiroaki The University of Tokyo, The University of Tokyo Hospital, Lecturer (60251295)
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| Co-Investigator(Kenkyū-buntansha) |
TAKEUCHI Takumi The University of Tokyo, The University of Tokyo Hospital, Associate Professor (90167487)
HIRATA Yaunobu The University of Tokyo, The University of Tokyo Hospital, Associate Professor (70167609)
KITAMURA Tadaichi The University of Tokyo, The University of Tokyo Hospital, Professor (70010551)
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| Project Period (FY) |
2006 – 2007
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| Keywords | Erectile dysfunction / athelosclerosis / microarray assay / pulse wave velocity |
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| Research Abstract |
Erectile dysfunction is mainly due to the inability of the cavernosal smooth muscle of the penis to undergo complete relaxation. In the aging rat model, erectile dysfunction is accompanied by a reduction of penile smooth muscle compliance and, in very old animals, by a decrease in penile nitric oxide synthase (NOS), which is responsible for the synthesis of the mediator of penile erection, nitric oxide (NO).
we examined alterations in penile gene expression in diabetic rats and littermate controls. With the use of Affymetrix GeneChip arrays and statistical filtering. Athelosclerosis related genes cause vascular endothelial dysfunction and is a major risk factor for cardiovascular diseases. The data from this study are relevant to understanding the mechanisms underlying the pathophysiological effect of microcirculation disorder, particularly on endothelial function and pathogenesis of atherosclerosis. CYP3A correlated information about inactivating action of estrogen/testosterone has close relationship with erectile dysfunction and LOH conditions. The data suggest that a significant inverse relation exists between presumed atherosclerotic load (as assessed by the number of erectile dysfunction risk factors and events) and aortic compliance determined noninvasively based on aortic pulse wave velocity measurements. Erectile dysfunction risk shows outward symptom during the early stage of cardiovascular risk factors. If these findings are confirmed by prospective, longitudinal follow-up studies, such measurements may prove useful as a noninvasive marker of vascular risk.
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