| Project/Area Number |
25860879
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pediatrics
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| Research Institution | Wakayama Medical University |
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Principal Investigator |
Hama Taketsugu 和歌山県立医科大学, 医学部, 博士研究員 (00508020)
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| Project Period (FY) |
2013-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2014: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 多発性嚢胞腎 / fibrocyte / 線維化 / CPKマウス / ARPKD / 繊維化 |
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| Outline of Final Research Achievements |
The pathophysiology of cystic epithelia in polycystic kidney disease (PKD) is characterized by altered proliferative activity, a secretory rather than absorptive function, and an abnormal matrix microenvironment. However, the aspect of extracellular matrix abnormality, especially fibrosis, has not been fully investigated in PKD. Recently, circulating fibrocytes expressing both leukocyte and mesenchymal antigens have been clarified to have a key role of progressing fibrosis in any organ. Therefore, we investigate fibrocytes contribution in cpk mouse.As a result, collagen type I gene level expressed significantly higher in cpk mice than control. CD45 and collagen dual-positive cells were detected predominantly in cpk mice. These findings suggested that fibrocytes were recruited in cpk and participated in the progression of fibrosis. Therefore, they may be new targets for a disease-specific intervention.
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