| Co-Investigator(Kenkyū-buntansha) |
OGAWA Yoshihiro Kyoto University, Graduate School of Medicine, Instructor, 医学研究科, 助手 (70291424)
ITOH Hiroaki Kyoto University, Graduate School of Medicine, Instructor, 医学研究科, 助手 (70263085)
KARIYA Masatoshi Kyoto University, Graduate School of Medicine, Lecturer, 医学研究科, 講師 (90243013)
SAITOH Yoshihiko Nara Medical University, Professor, 医学部, 教授 (30250260)
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| Research Abstract |
The aim of this study was to analyze the pathophysiology of intrauterine growth restriction from the view point of cell biology of the placenta. The endothelial and inducible isoforms of nitric oxide (NO) synthesizing enzyme (eNOS, INOS) were abundantly expressed in the intrauterine tissues, especially in the placental trophoblast cells. The expression of eNOS and iNOS in the placenta ore stable even after the onset of labor, suggesting that these enzymes may play some roles in the maintenance of blood flow under the influence of other vasoconstrictive substances such as prostaglandins and angiotensin II during parturision.
The aim of present study is to develop an animal model of bone marrow cells transfer into mouse placenta in the mid gestation. Mono-nuclear fraction of bone marrow cells from GFP-Tg mice (1-5x10^5 cells/3ml) were directly injected into placental portion. The 1-8% of serial section (150-200 plates/placenta) of the sampled placenta showed 1-8 GFP positive cells, approx
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imately 5% of which were positive for cytokeratin, CD34 or p57kip2, suggesting that this experimental model might be useful in the investigation of developmental process of the placenta.
Resistin, a novel peptide hormone, is specifically expressed in the adipose tissue and decreases insulin sensitivity in rodents. In the present study, we demonstrate resistin gene expression in the human placental tissue, mainly in trophoblastic cells. The resistin gene expression in term placental tissue was more prominent than was seen in the first trimester chorionic tissue. Thus, resistin is a newly isolated placental hormone in humans which may modulate insulin sensitivity during pregnancy.
We also investigated the expression of leptin, resistin and adiponectin in the growth-restricted fetuses using mouse model of maternal food restriction. Food restriction produced IUGR fetuses. Expressions of leptin, resistin, adiponectin in IUGR fetuses were approximately half of the control fetuses. The IUGR newborn rapidly catch-up the control newborn under breast feeding ad libitum, but the leptin mRNA expression in the skin of these newborns was significantly elevated as compared to that of control newborns. Less
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