The roles of STAT5B for gene regulation on human CD4+ T cells

Research Project

Project/Area Number	25460697
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	Laboratory medicine
Research Institution	Jichi Medical University
Principal Investigator	Kanai Takahiro 自治医科大学, 医学部, 講師 (00398504)
Co-Investigator(Kenkyū-buntansha)	Odaka Jun 自治医科大学, 医学部, 講師 (70382885) Aoyagi Jun 自治医科大学, 医学部, 助教 (80438639)
Project Period (FY)	2013-04-01 – 2016-03-31
Project Status	Completed (Fiscal Year 2015)
Budget Amount *help	¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000) Fiscal Year 2015: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000) Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000) Fiscal Year 2013: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Keywords	小児特発性ステロイド感受性ネフローゼ症候群 / T細胞 / 遺伝子工学 / STAT5B / CD4+T細胞 / CD4+ T 細胞 / 川崎病
Outline of Final Research Achievements	We revealed several genes that were regulated by STAT5B on human T cells. Some of the genes were corresponding to the phenotype of idiopathic steroid-sensitive nephrotic syndrome in children. When we analyzed the serum from the patients with idiopathic steroid-sensitive nephrotic syndrome, a substance was found which serum levels were associated with urinary protein/urinary creatinine levels. This is the first time to report the association of the substance and the status of idiopathic steroid-sensitive nephrotic syndrome. In next step, we are planning to find how the substance effects on the pathophysiology of idiopathic steroid-sensitive nephrotic syndrome.