Project/Area Number |
21591381
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Pediatrics
|
Research Institution | The University of Tokyo |
Principal Investigator |
MIURA Kenichir 東京大学, 医学部附属病院, 助教 (70408483)
|
Co-Investigator(Kenkyū-buntansha) |
IGARASHI Takashi 東京大学, 医学部附属病院, 教授 (70151256)
SEKINE Tattshl 東邦大学, 大橋病院, 教授 (50255402)
|
Project Period (FY) |
2009 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | 小児腎 / 泌尿器学 / ネフローゼ / 細胞・組織 / 生体分子 / 臨床 / 蛋白質 / ポドサイト / スリット膜 / 分子複合体 / シグナル伝達 / MYH9 / NMMHC-IIA / 巣状糸球体硬化症 |
Research Abstract |
MYH9 encodes nonmuscle myosin heavy chain-IIA(NMMHC-IIA) and causes Epstein syndrome characterized by macrothrombocytopenia, sensorineural hearing loss, and progressivc renal failure(focal segmental glomerulosclerosis ; FSGS). Recent studies have revealed that MYH9 polymotthiSms are associatcd with adult FSGS and progressive renal failurc. FSGS is a leading cause of refractory nephrotic syndrome in children, and, ve investigated animal and human renal specimens to deterlnine whether NMMHC-IIA was involved in development of FSGS. Electron microscopy immunogold labeling sttdies revealcd that NMMHC-IIA was located primarily at primaly proccsseS of podocytes. Immunohistochemical analysis revealed that the expresslon lcvel of NMMHC-IIA markedly decreased in steroid-resistant FSGS, whereas it did not change in chronic glomeruloncphritis, with heavy proteinuria A marked decrease in the expresslon level of NMMHC-IIA、was also obsetted in the glomerulus of puromycin aminonucleoside-trcatcd rat, which presents、with nephrotic syndrome. Thcse results suggest that NMMHC-IIA has an important role in dcvelopment of proteinuria in idiopathic nephrotic syndrome and architectural maintenance of podocytes.
|