Project/Area Number |
23591188
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Kidney internal medicine
|
Research Institution | Nagoya University |
Principal Investigator |
KOSUGI TOMOKI 名古屋大学, 医学(系)研究科(研究院), 助教 (90584681)
|
Co-Investigator(Kenkyū-buntansha) |
MARUYAMA Shoichi 名古屋大学, 大学院医学系研究科, 准教授 (10362253)
佐藤 和一 名古屋大学, 医学部附属病院, 講師 (90508920)
|
Co-Investigator(Renkei-kenkyūsha) |
SATO Waichi 名古屋大学, 医学部附属病院, 講師 (90508920)
|
Project Period (FY) |
2011 – 2013
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
|
Keywords | CD147/Basigin / ループス腎炎 / 糖尿病性腎症 / CD147 / ATP産生 / Glucose代謝 / インスリン抵抗性 / Lupus腎炎 / 補体C3活性 / 抗dsDNA抗体 / 免疫複合体 / CD147 / 補体C3活性 / 抗ds-DNA抗体 |
Research Abstract |
CD147/Basigin, a glycosylated transmembrane protein, plays important roles of cell survival, invasion and metastasis. With regard to diabetes and autoimmune diseases, however, the molecular mechanism involving CD147 remains unknown. As CD147 identifies activated regulatory T cell (Treg), the attention has become extended to the autoimmune diseases. Interleukin (IL)-17 producing T cell and Treg also serve important roles in the pathogenesis of SLE. In the present study, lack of CD147 promotes Th17 differentiation through the STAT3 activation, eventually leading to the development of lupus nephritis. On the other hand, CD147 play deleterious effects in renal inflammation caused by ischemia and renal fibrosis through the enhanced infiltration of inflammatory cells. Diabetes is also influenced by CD147 in renal inflammation. Our results may shed light on the mechanisms underlying the pathogenesis of diabetes nephropathy and lupus nephritis.
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