The regulation of fibrosis and calcification by gadolinium

Research Project

Project/Area Number	24790146
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	Medical pharmacy
Research Institution	Gunma University
Principal Investigator	YAMADA Kazuya 群馬大学, 医学部附属病院, 助教 (90420190)
Research Collaborator	MOTEGI Sei-ichiro 群馬大学, 大学院医学系研究科, 講師 (20420185)
Project Period (FY)	2012-04-01 – 2014-03-31
Project Status	Completed (Fiscal Year 2013)
Budget Amount *help	¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000) Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000) Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Keywords	腎性全身性線維症 / ガドリニウム / 間葉系幹細胞 / 石灰化 / 腎性全身線維症 / 細胞内シグナル
Research Abstract	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. ET-1/ET receptor expression and phosphorylation of PDGF receptor, ERK and Aktin human mesenchymal stem cells (MSC) treated with Gd were elevated, suggeting that Gd induces proliferation and calcification of hMSC via enhancement of ETR signaling and/or PDGFR signaling and ERK and Akt pathway.