Project/Area Number |
26462671
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Ophthalmology
|
Research Institution | St. Marianna University School of Medicine |
Principal Investigator |
Takagi Hitoshi 聖マリアンナ医科大学, 医学部, 教授 (70283596)
|
Co-Investigator(Kenkyū-buntansha) |
北岡 康史 聖マリアンナ医科大学, 医学部, 准教授 (10367352)
宗正 泰成 聖マリアンナ医科大学, 医学部, 講師 (30440340)
|
Co-Investigator(Renkei-kenkyūsha) |
TAKAKURA Nobuyuki 大阪大学, 微生物学研究所, 教授 (80291954)
KOYA Daisuke 金沢医科大学, 医学部, 教授 (70242980)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
Keywords | オートファジー / 糖尿病網膜症 / 網膜血管細胞死 |
Outline of Final Research Achievements |
Vascular cell death causes diabetic retinopathy and autophagy has been paid attention as a novel cell death mechanism. We compared gene expression between low and high glucose - stimulated vascular endothelial cells. High glucose-stimulation induced inflammatory and thrombotic effects in gene expression profile in vascular cells. TGFB2 specially upregulated and mediated cell death. High glucose condition upregulated autophagy and inhibited TNF-induced P62 increase, which are reversed by inhibition of autophagy reflux. These finding suggests that autophagy regulation could be applied to future treatment strategies.
|