Project/Area Number |
11671619
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Obstetrics and gynecology
|
Research Institution | Kobe University |
Principal Investigator |
MATSUO Hiroya Kobe University of School of Medicine, OB/GY, associated Professor, 医学部・附属病院, 助教授 (60229432)
|
Co-Investigator(Kenkyū-buntansha) |
MARUO Takeshi Kobe University of School of Medicine, OB/GY, Professor, 医学部, 教授 (60135811)
佐本 崇 神戸大学, 医学部, 助手 (80294213)
|
Project Period (FY) |
1999 – 2000
|
Project Status |
Completed (Fiscal Year 2000)
|
Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2000: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1999: ¥2,000,000 (Direct Cost: ¥2,000,000)
|
Keywords | Torophoblast / Cytotrophoblast / Syncytiotrophoblast / Extravillous trophoblast / Apoptosis / Proliferation / Differentiation / Preeclampsia / 胎盤 / bcl-2 / PPAR / 脱落膜 / 甲状腺ホルモン / トロホブラスト / PCNA / Bcl-2蛋白 / IUGR / PIH |
Research Abstract |
In order to evaluate placental trophoblast proliferation and apoptosis during pregnancy, we have determined proliferating cell nuclear antigen (PCNA) expression, apoptotis and Bcl-2 protein expression in the human placenta over the course of pregnancy. The very early 4 to 5 weeks placenta is characterized by highly proliferative activity of C-cells associated with increased occurrence of apoptosis of both C-cells and S-cells and that proliferative activity of C-cells as well as apoptosis of both C-cells and S-cells are markedly diminished after 7 weeks of pregnancy. A little occurence of apoptotis in S-cells in term placentas is congruent with the observation that Bcl-2 protein expression in S-cells increased with the advance of pregnancy. The abundant expression of Bcl-2 protein in differentiated S-cells may be one of the mechanisms to protect S-cells from the process of apoptosis in term placentas. There are two local subtypes of extravillous trophoblast (EVT) : proliferative phenotype EVT and invasive phenotype EVT.The mechanism of invasion of EVT to the decidua remains obscure. In order to elucidate the potential role of apoptosis in regulating the invasion of EVT to the decidua, we have assessed the expression of apoptosis-regulating proteins, Fas antigen (Fas), Fas-ligand (Fas-L) and Bcl-2 protein, and apoptosis in the proliferative phenotype EVT and the invasive phenotype EVT at term (37 to 38 weeks). The present findings suggest that apoptosis in EVT may play a vital role in regulating the invasion of EVT to the decidua. It seems likely that Fas/Fas-L and Bcl-2 protein expression participate in the regulation of apoptosis in EVT and that the increased occurrence of apoptosis in the invasive phenotype EVT may be attributable to the increased expressions of Fas and Fas-L and decreased expression of Bcl-2 protein in those cells.
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