Project/Area Number |
25462517
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Urology
|
Research Institution | Fukushima Medical University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
Kushida Nobuhiro 福島県立医科大学, 医学部, 助教 (30381396)
Haga Nobuhiro 福島県立医科大学, 医学部, 助教 (50586617)
Kojima Yoshiyuki 福島県立医科大学, 医学部, 教授 (60305539)
Aikawa Ken 福島県立医科大学, 医学部, 準教授 (80295419)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2013: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
|
Keywords | 尿道部分閉塞 / HIF-1 / p53 / 膀胱 / 低酸素 / 虚血 / 閉塞膀胱 / p53 / 前立腺肥大症 / 下部尿路通過障害 / 膀胱収縮障害 / 血管新生 |
Outline of Final Research Achievements |
Bladder hypertrophy occurs as a compensatory response to infravesical obstruction, such as benign prostatic hyperplasia (BPH). However, this condition may also be an indication of ongoing pathogenic processes and entrance into a decompensatory stage. In addition, ischemia is also known to induce in men with bladder outlet obstruction as a result of BPH. This study has shown that hypoxia induces the expression of HIF-1 mRNA and encourages angiogenesis in bladder tissue. In addition, continuous hypoxia induces the expression of p53 mRNA and suppresses the expression of HIF-1 mRNA in bladder tissue. Taken together, our study suggests that p53 breaks down compensatory mechanism for hypoxia in the bladder, and then result in detrusor contractile dysfunction.
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