| Project/Area Number |
24591245
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | University of Occupational and Environmental Health, Japan |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SERINO Ryota 産業医科大学, 大学病院, 講師 (00309957)
MIYAMOTO Tetsu 産業医科大学, 医学部, 非常勤医師 (30611305)
KABASHIMA Narutoshi 産業医科大学, 大学病院, 非常勤医師 (80279322)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 腹膜透析 / 慢性腎不全 / 透析液 / 生体適合性 / 細胞接着 / 国際情報交換（米国） |
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| Outline of Final Research Achievements |
Long-term peritoneal dialysis (PD) is associated with the development of functional and structural alterations of the peritoneal membrane, and is eventually limited by reduced efficacy. We have shown that high glucose concentrations inhibit FAK-mediated migration of mesothelial cells, and that dialysates containing high glucose concentrations cause peritoneal damage by inhibiting wound healing of the mesothelial cell monolayer. We also showed that an integrin-activating peptide, PHSRN, ameliorates inhibitory effects of conventional peritoneal dialysis fluids on peritoneal wound healing. We elucidated that PHSRN recoveres glucose-induced inhibition of cell motility and phosphorylation of focal adhesion kinase and its downstream p130Cas.
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