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2014 Fiscal Year Final Research Report

Molecular mechanism on the formation and renewal of slit membranes of glomerular podocyte

Research Project

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Project/Area Number 24591214
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Kidney internal medicine
Research InstitutionJuntendo University

Principal Investigator

KURIHARA HIDETAKE  順天堂大学, 医学部, 准教授 (80311976)

Co-Investigator(Kenkyū-buntansha) ICHIMURA Koichiro  順天堂大学, 医学部, 准教授 (10343485)
Project Period (FY) 2012-04-01 – 2015-03-31
Keywords腎臓学 / 足細胞 / 糸球体濾過 / 細胞接着 / ネフローゼ
Outline of Final Research Achievements

The slit diaphragm (SD) plays an important role in permeability barrier function. We have identified several molecules associated with the formation and renewal of SD. 1) To assess the function of MAGI-1, we analyzed the podocyte-specific MAGI-1 deficient mice and found that the deletion of MAGI-1 caused the decrease of SD molecules at the plasma membrane. In addition, exocytosis of nephrin molecule is inhibited by podocyte-specific deletion of aPKC. Data indicate that both molecules are associated with the turnover of SD. 2) We have found that myosin 1e is tightly associated with the tight junction which moves from the apex to the base of immature podocyte during the development. Myosin 1e is also involved in the SD formation. Recently, we have determined that KIF11 is tightly associated with tight junctions of renal epithelial cells in vivo and in vitro. Calcium switch experiment and silencing of KIF11 indicate that KIF11 is involved in the tight junction formation.

Free Research Field

細胞生物学

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Published: 2016-06-03  

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