| Project/Area Number |
20591285
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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 |
Pediatrics
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| Research Institution | Wakayama Medical University |
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Principal Investigator |
NAKANISHI Koichi Wakayama Medical University, 医学部, 講師 (50336880)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIKAWA Norishige 和歌山県立医科大学, 医学部, 教授 (10158412)
IZUMI Genkichi 和歌山県立医科大学, 医学部, 博士研究員 (70423952)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2008: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 多発性嚢胞腎 / 遺伝性腎疾患 / 上皮間葉移行 / PCKラット / 間葉系マーカー / E-cadherin / β-catenin / N-cadherin |
|---|
| Research Abstract |
We examined the expression of cell adhesion molecules and mesenchymal markers to clarify a role of EMT in PCK rat, an ARPKD model with a mutation in the orthologue of human PKHD1. E-cadherin and β-catenin expression levels in cystic tubule was attenuated and localized to lateral cell-cell contacts according to cyst enlargement in PCK rats. Some epithelial cells in large cysts derived from these segments of nephron, especially in adjacent fibrotic area, showed positive immunoreactivity of vimentin and fibronectin. Vimentin and fibronectin positive cells are increased in fibrotic area around cyst. In conclusions, these findings suggested that EMT is involved in pathophysiology of PKD.
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