Research on molecular mechanism of nephrotic syndrome

2014 Fiscal Year Final Research Report

• Project/Area Number: 24591569
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Pediatrics
• Research Institution: The University of Tokyo
• Principal Investigator: MIURA Kenichiro 東京大学, 医学部附属病院, 助教 (70408483)
• Co-Investigator(Kenkyū-buntansha): SEKINE Takashi 東邦大学, 医学部, 教授 (50255402) ; IGARASHI Takashi 独立行政法人国立成育医療研究センター, 総長 (70151256)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 小児腎・泌尿器学

Outline of Final Research Achievements

It remains to be elucidated how idiopathic nephrotic syndrome including focal segmental glomerulosclerosis (FSGS) develops, while glomerular podocyte cytoskeletal proteins have recently emerged as candidate molecules associated with development of proteinuria. Mutations in the MYH9 gene, which encodes nonmuscle myosin heavy chain-IIA (NMMHC-IIA), cause Epstein syndrome and secondary FSGS in the kidney.
Firstly, we showed that NMMHC-IIA was localized at primary processes of the podocyte. Secondly, podocyte expression of NMMHC-IIA decreased specifically in Epstein syndrome and idiopathic nephrotic syndrome including primary FSGS. Thirdly, expression of other podocyte-associated proteins did not significantly changed in both FSGS and other chronic glomerulonephritis. These results suggest that NMMHC-IIA is strongly associated with development of idiopathic nephrotic syndrome, playing a pivotal role in maintenance of podocyte cytoskeleton.

Free Research Field

医歯薬学