| Project/Area Number |
15390270
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Osaka University |
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Principal Investigator |
IMAI Enyu Osaka University, Graduate School of Medicine, Associate Professor, 医学系研究科, 助教授 (00223305)
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| Co-Investigator(Kenkyū-buntansha) |
ITO Takahito Osaka University, Graduate School of Medicine, Assistant Professor, 医学系研究科, 助手 (60362703)
ISAKA Yoshitaka Osaka University, Graduate School of Medicine, Associate Professor, 医学系研究科, 助教授 (00379166)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥15,100,000 (Direct Cost: ¥15,100,000)
Fiscal Year 2004: ¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 2003: ¥13,000,000 (Direct Cost: ¥13,000,000)
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| Keywords | kidney / regenerative medicine / GFP / PDGF / SP cell / fetal microchimerism / 幹細胞 / マイクロキメリズム / 肝臓 / 妊娠 / ネフロン / 概日リズム / 骨髄 / レチノイン酸 / ネフリン |
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| Research Abstract |
1)We found the biological condition under which bone marrow-derived cells differentiate into glomerular mesangial cells. 2)We purified SP cells from kidney, and characterized them. 3)We demonstrated that fetal cells were engragted in mother rats as a result of fetal microchimerism, and that the cells contributed to the repair of liver and kidney after chronic injury. Reportedly, pregnant women carry fetal cells which are imported through placenta. These fetal cells survive and exist for a long time in women with the history of pregnancy. This phenomenon is called fetal microchimerism. In human, there is a case with 27-year longstanding microchimerism. It is reported that fetal cells are detected in chronic inflammation lesions such as chronic thyroiditis and hepatitis C. Because fetal cells are semi-allogenic to mothers, they might cause autoimmune diseases such as Sjogren syndrome and scleroderma. We studied the relation between fetal cells in mother rats and renal diseases. In rat gentamcin-induced nephropathy, we found fetal cells were incorporated into tubular epithelial structure. This result suggests that human fetal cells also contribute to mother kidney. 4)We established a method to identify molecules which are involved in the repair of glomerular epithelial cells. 5)We found that retinoic acid plays a relevant role in the repair and that retinoic acid facilitates transcription of nephrin.
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