| Project/Area Number |
26670713
|
|---|
| Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Obstetrics and gynecology
|
|---|
| Research Institution | The University of Tokyo |
|---|
Principal Investigator |
HIROTA YASUSHI 東京大学, 医学部附属病院, 講師 (40598653)
|
|---|
| Project Period (FY) |
2014-04-01 – 2015-03-31
|
| Project Status |
Completed (Fiscal Year 2014)
|
| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2014: ¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
|
|---|
| Keywords | 細胞老化 / 組織恒常性 / マクロファージ / 子宮 / 分娩 / 組織リモデリング / マウスモデル / p53 |
|---|
| Outline of Final Research Achievements |
Cellular senescence, defined as an irreversible cell cycle arrest, affects the tissue microenvironment. Our previous study demonstrated the presence of uterine cellular senescence in preterm delivery, suggesting its involvement in uterine dysfunction. In the current study, we showed abundant senescent cells in the postpartum uterus and their gradual disappearance. Macrophages were present specifically around the area rich in senescent cells. The depletion of macrophages in the puerperal mice after normal parturition using anti-F4/80 antibody enlarged the area with senecent cells in the uterus. In addition, excessive senescent cells were observed in the uterus after preterm birth in p53 conditional knockout mice, and their second pregnancy rate immediately after the first delivery was significantly decreased. These findings indicate that there is a physiological system for removal of senescent cells after parturition, and its disruption is associated with uterine pathology.
|
