| Project/Area Number |
24591192
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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 | Kanazawa University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
WADA Takashi 金沢大学, 医学系, 教授 (40334784)
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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: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 糖尿病性腎症 / 免疫担当細胞 / 慢性炎症 / 炎症性疾患 / 炎症・免疫 / 腎固有細胞 / 糖尿病 |
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| Outline of Final Research Achievements |
High glucose (HG) stimulates various kinds of leukocytes, resulting in an abberant the inflammatory/anti-inflammatory immune balance. However, it is unclear if renal resident cells showed an abberant immune balance in diabetic nephropathy (DN). Therefore, we hypothesized that the aberrant immune balance of renal resident cells contributes to the pathogenesis of DN. To explore this possibility, we performed genome-wide transcriptome profiling in mesangial cells and tubular epithelial cells (TECs), which were stimulated by HG and detected the expression of inflammation associated genes. Pro-inflammatory/Th1 gene expression was upregulated, but Th2 related gene expression was downregulated in mesangial cells. In TECs, HG stimulation increased pro-inflammatory/Th1/Th2 gene expression. The data taken together indicate that HG shifts the immune balance toward pro-inflammatory/Th1 phenotype in renal resident cells, which might initiate and/or prolong inflammation.
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