Discovery of a molecular switch for progressive bladder dysfunction

2015 Fiscal Year Final Research Report

• 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: Matsuoka Toshimitsu 福島県立医科大学, 医学部, 研究員 (60528280)
• 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
• Keywords: 尿道部分閉塞 / HIF-1 / ｐ５３ / 膀胱 / 低酸素 / 虚血

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.

Free Research Field

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