2006 Fiscal Year Final Research Report Summary
Study of placental formation and functional differentiation by tissue specific stem cell transplantation
| Project/Area Number |
17591728
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Kyoto University |
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Principal Investigator |
SUZUKI Ayako Kyoto University, Graduate School of Medicine, assistant professor, 医学研究科, 助手 (90378696)
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| Co-Investigator(Kenkyū-buntansha) |
ITOH Hiroaki Kyoto University, Graduate School of Medicine, lecturer, 医学研究科, 講師 (70263085)
YURA Shigeo Kyoto University, Graduate School of Medicine, assistant professor, 医学研究科, 助手 (60335289)
SAGAWA Norimasa Mie University, Graduate School of Medicine, professor, 医学系研究科, 教授 (00162321)
SUZUKI Yoshihisa Kyoto University, Graduate School of Medicine, associate professor, 医学研究科, 助教授 (30243025)
ITOH Hiroshi Kyoto University, Graduate School of Medicine, associate professor, 医学研究科, 助教授 (40252457)
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| Project Period (FY) |
2005 – 2006
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| Keywords | IUGR / placenta / mononuclear cell / glucocorticoid / fetal growth |
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| Research Abstract |
The placenta plays an essential role in the growth of fetus in the uterus. Any insult in placental development, such as abnormal immune reaction or maternal malnutrition, can result in poor placental growth and placental insufficiency. In the present study, we evaluated an involvement of maternal bone-marrow derived mononuclear cells in the development of the placenta by transplanting these cells in growing placenta. Bone-marrow cells obtained from GFP transgenic mice were injected in the growing placenta and was observed to be retained in the placental tissue just prior to delivery. Moreover, GFP positive maternal mononuclear cells were observed in the placenta of non-GFP pups growing in the uterus of GFP transgenic dams, thus indicating that maternal mononuclear cells may contribute somehow to the formation of the placenta. In the present study, we also elucidated an involvement of glucocorticoid inactivating enzyme, 11 beta-hydroxysteroid dehydrogenase type 2(11βHSD2). 11βHSD2 was expressed in chorionic epithelium of the mouse placenta. 11βHSD2 expression in the placenta was increased by maternal food restriction during pregnancy. Therefore, it is implicated that fetus is protected from exposure to glucocorticoid in maternal circulation increased by food restriction stress. In addition, placental 11βHSD2 expression was further increased by feeding high protein diet during food restriction, together with improved fetal growth. These findings may give us a clue to develop a new strategy to have a good fetal outcome.
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