2014 Fiscal Year Final Research Report
Pathogenesis of immune cells in progressive kidney disease
| Project/Area Number |
24591192
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Kidney internal medicine
|
|---|
| Research Institution | Kanazawa University |
|---|
Principal Investigator |
|
|---|
| 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
|
