Novel strategy for the treatment of active nephritis using secreted FSP1
Project/Area Number |
24390216
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Partial Multi-year Fund |
Section | 一般 |
Research Field |
Kidney internal medicine
|
Research Institution | University of Fukui |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
KIMURA Hideki 福井大学, 医学部附属病院, 准教授 (20283187)
OKADA Hirokazu 埼玉医科大学, 医学部, 教授 (60233342)
NAKATANI Kimihiko 奈良県立医科大学, 医学部, 非常勤講師 (80398445)
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥17,810,000 (Direct Cost: ¥13,700,000、Indirect Cost: ¥4,110,000)
Fiscal Year 2014: ¥6,630,000 (Direct Cost: ¥5,100,000、Indirect Cost: ¥1,530,000)
Fiscal Year 2013: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2012: ¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
|
Keywords | FSP1 / ポドサイト / TLR4 / 治療薬 / 糸球体腎炎 / メサンギウム細胞 / 半月体 |
Outline of Final Research Achievements |
FSP1-positive podocytes were observed in active glomerular damage. In this study, we investigated whether secreted FSP1 from podocytes has some biological effects on mesangial cells in vitro and in vivo. We generated recombinant FSP1 (rFSP1) by the standard method. rFSP1 inhibited LPS-induced TNF-α, IL-6, and MCP-1 production and mRNA expression in cultured mesangial cells. LPS injection induced glomerular TNF-αmRNA expression in vivo and this induction was significantly inhibited by the peritoneal injection of rFSP1. Next, we generated transgenic mice (FSP1.TG) in which podocyte-specific overexpressions of FSP1 were observed. LPS-induced glomerular TNF-α expression in FSP1.TG mice was significantly suppressed as compared with control wild mice. These results suggest that secreted FSP1 has renoprotective effects and plays a role in podocyte-mesangial crosstalk.
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Report
(4 results)
Research Products
(9 results)