| Project/Area Number |
14571557
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Obstetrics and gynecology
|
|---|
| Research Institution | Osaka University |
|---|
Principal Investigator |
KOYAMA Masayasu (2003) Osaka University Graduate School of Medicine, Associate Professor, 医学系研究科, 助教授 (00183351)
井阪 茂之 (2002) 大阪大学, 医学系研究科, 助手 (50346201)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
TSUTSUI Tateki Osaka University, Graduate School of Medicine, Assistant Professor, 医学系研究科, 助手 (00294075)
SHIMOYA Koichiro Osaka University, Graduate School of Medicine, Assistant Professor, 医学系研究科, 助手 (40291950)
KIMURA Tadashi Osaka University, Graduate School of Medicine, Assistant Professor, 医学系研究科, 助手 (90240845)
TSUJIE Tomoko Osaka University, Graduate School of Medicine, Assistant Professor, 医学系研究科, 助手 (50362695)
古山 将康 大阪大学, 医学系研究科, 助教授 (00183351)
|
|---|
| Project Period (FY) |
2002 – 2003
|
| Project Status |
Completed (Fiscal Year 2003)
|
| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2003: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2002: ¥1,800,000 (Direct Cost: ¥1,800,000)
|
|---|
| Keywords | trophoblasts / preeclampsia of pregnancy / oxidative stress / cell cycle, cyclin / cyclin / HNE / COX-2 / lipid peroxide catabolite / 子宮内膜 / サイクリン依存性キナーゼ / サイクリン依存性キナーゼインヒビター |
|---|
| Research Abstract |
Manifestation analysis of a cell cycle related proteins of trophoblasts in abnormal pregnancy
We obtained chorionic tissues of molar pregnancy, early normal pregnancy, preterm pregnancy andfull-term pregnancy with informed consents at delivery, and we extracted protein and embedded tissues in conventional paraffin. In normal trophoblastic villous cells of each trimester of pregnancy and hydatidiform mole, we confirmed manifestation of cell cycle related proteins such as PCNA, CDK2, p21, p27, p57 and Cyclin Eby Western blot analysis. PCNA, CDK2 and Cyclin Eproteins were strongly expressed in hydatidiform mole and early gestational trophoblasts at the same level. With the late gestation period, the expression of these proteins was diminished. As for p21 which we showed high manifestation in normal trophoblasts of early pregnancy, and deteriorated in the latter period, its stronger expression was found in hydatidiform mole than early pregnancy trophoblasts. As for p57 which is expressed in
… More
the normal placenta, the manifestation was not found in hydatidiform mole. As for p27 which manifestation enhanced in normal trophoblasts at the early trimester and getting weaker in the latter period, strong manifestation was found in hydatidiform mole than a late gestational trophoblasts. We investigated the localization of p21, p27, p57 in hydatidiform mole by immunohistochemical analysis and compared its localization with the normal gestational trophoblasts.
Analysis of influence of oxidative stress in gestational trophoblastic tissue
We obtained placentae at the time of a full-term pregnancy and preterm labor and extracted RNA, protein, and encapsulated a part of these tissues in paraffin. Accumulation of 4hydroxy-2nonenal (HNE), the catabolite of peroxide lipid produced by oxidative stress was investigated by Immunohistochemical staining and Western blot analysis. As for the trophoblastic tissue obtained from the patient suffering from preeclampsia, accumulationof 1-INEwas remarkable in comparison with trophoblastic tissue without any complication. In the same manner, accumulation of HNE was significantly remarkable in trophoblastic tissue with chorioamnionits. We supplemented HNE in cultured trophoblastic tissue and investigated the expression of cyclooxygenase-2 (COX-2) by RT-PCR and Western blot analysis. COX-2 was expressed at transcriptional and translational level at increased for level at time and concentration dependent manner. Production of Prostaglandin also increased at the time dependent manner. These results indicated that trophoblastic tissue caught oxidative stress produced lipid peroxide catabolite increased and activate the cascade of prostaglandin synthetic system. Less
|
