2020 Fiscal Year Final Research Report
Sleep apnea syndrome induces clock gene abnormalities and causes nocturia in the mice bladder
Project/Area Number |
19K18579
|
Research Category |
Grant-in-Aid for Early-Career Scientists
|
Allocation Type | Multi-year Fund |
Review Section |
Basic Section 56030:Urology-related
|
Research Institution | University of Yamanashi |
Principal Investigator |
IHARA Tatsuya 山梨大学, 大学院総合研究部, 助教 (90622407)
|
Project Period (FY) |
2019-04-01 – 2021-03-31
|
Keywords | 夜間頻尿 / 睡眠時無呼吸症候群 / 時計遺伝子 |
Outline of Final Research Achievements |
SAS loading increased the frequency of mouse voiding during sleep. In addition, bladder capacity also decreased after SAS loading. These results indicated that SAS could induces nocturia-like pathology in mice. As for the clock gene Per2 expression rhythm in cultured cells of bladder epithelium after hypoxic stimulation, a circadian rhythm similar to that of control was observed with 10% hypoxic stimulation. However, the circadian rhythm changed as the oxygen concentration was lowered to 5% and 1%. The circadian Per2 expression disappeared completely with 1% hypoxic stimulation. From these results, SAS loading may cause nocturia through abnormal circadian rhythm of the bladder.
|
Free Research Field |
泌尿器科
|
Academic Significance and Societal Importance of the Research Achievements |
SSASの慢性的な低酸素ストレスが膀胱の時計遺伝子異常を介し夜間頻尿を惹起させる。いままで言われてこなかった新しい病態の一つであり、夜間頻尿に対する新規の治療戦略、新規治療薬の創生に結び付く可能性がある。
|