2016 Fiscal Year Final Research Report
Role of HMGA1 on the pathogenesis of preeclampsia
| Project/Area Number |
26462493
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Obstetrics and gynecology
|
|---|
| Research Institution | Ehime University |
|---|
Principal Investigator |
|
|---|
| Research Collaborator |
Yamamoto Sawa
|
|---|
| Project Period (FY) |
2014-04-01 – 2017-03-31
|
| Keywords | 妊娠高血圧症候群 / 血管内皮 / 絨毛細胞 / 高血圧 |
|---|
| Outline of Final Research Achievements |
On the third day after the implantation, trophoblastic cells were aggregated around the embryo and HMGA1 was observed in the cytoplasm as well as the nuclei derived from the preeclampsia model mouse. A part of HMGA1 was also released out of the cells by the implantation site. Furthermore, HMGA1 was transported into the cytoplasm from the nuclei in the human preeclamptic placenta. We demonstrated that DCA could stimulate the transportation of HMGA1 from nuclei to cytoplasm. In culture system, DCA decreased the proliferation and invasive capacity of extravillous trophoblast. In normal pregnancy, extravillous trophoblasts could invade into maternal decidua and uterine myometrium resulted in increased utero-maternal circulation to maintain the pregnancy. However, it is known that the effects were reduced in preeclampsia. Extra nuclear transport of HMGA1 is involved in the pathogenesis of preeclampsia through inhibiting extravillous trophoblasts invasion.
|
| Free Research Field |
周産期医学
|
