The mechanisms of skin fibrosis and calcification in nephrogenic systemic fibrosis
Project/Area Number |
25461662
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Dermatology
|
Research Institution | Gunma University |
Principal Investigator |
Ishikawa Osamu 群馬大学, 医学(系)研究科(研究院), 教授 (90168188)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | 腎性全身性線維症 / 皮膚線維化 / ガドリニウム / 間葉系幹細胞 / エンドセリン / 石灰化 |
Outline of Final Research Achievements |
Nephrogenic systemic fibrosis (NSF) is characterized by systemic fibrosis and abnormal calcification in patients with severe renal dysfunction. It is considered that gadolinium (Gd)-containing contrast agents used for magnetic resonance imaging trigger the development of NSF. However, the causative role of Gd and the mechanism of Gd-induced fibrosis and calcification in NSF are unknown.We conclude that Gd induces proliferation and calcification of human mesenchymal stem cells via enhancement of endothelin-1/endothelin receptor signalling. Our results contribute to understand the pathogenesis of NSF.
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Report
(4 results)
Research Products
(3 results)