Dysregulation of interaction between compound molecules in glomerular podocytes induces nephrotic syndrome
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.
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Report
(4 results)
Research Products
(71 results)
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[Journal Article] V2 vasoprcssin receptor(V2R) mutations in partial nephrogenic diabetes insipidus highlights protean agonism of V2R antagosists2012
Author(s)
Takahashi K, Makita N, Manaka K, Hisano M, Akioka Y, Miura K, Takubo N, Iida A, Ueda N, Hashimoto M, Fujita T, Igarashi T, Sekine T, Iiri T
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Journal Title
J Biol Chem
Volume: 287
Pages: 2099-2106
Related Report
Peer Reviewed
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[Journal Article] Patients with Epstein-Fechtner syndromes owing to MYH9 R702 mutations develop progressive proteinuric renal disease2010
Author(s)
Sekine T, Konno M, Sasaki S, Moritani S, Miura T, Wong WS, Nishio H, Nishiguchi T, Ohuchi MY, Tsuchiya S, Matsuyama T, Kanegane H, Ida K, Miura K, Harita Y, Hattori M, Horita S, Igarashi T, Saito H, Kunishima S
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Journal Title
Kidney Int
Volume: 78
Pages: 207-214
Related Report
Peer Reviewed
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