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2014 Fiscal Year Final Research Report

Pathogenesis of immune cells in progressive kidney disease

Research Project

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Project/Area Number 24591192
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Kidney internal medicine
Research InstitutionKanazawa University

Principal Investigator

IWATA Yasunori  金沢大学, 大学病院, 特任助教 (90432137)

Co-Investigator(Kenkyū-buntansha) WADA Takashi  金沢大学, 医学系, 教授 (40334784)
Project Period (FY) 2012-04-01 – 2015-03-31
Keywords糖尿病性腎症 / 免疫担当細胞 / 慢性炎症
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.

Free Research Field

腎臓病学

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Published: 2016-06-03  

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