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2014 Fiscal Year Final Research Report

An investigation of mechanism of progression of kidney disease using renal tubular cells differentiated from ES/iPS cells

Research Project

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Project/Area Number 24591211
Research Category

Grant-in-Aid for Scientific Research (C)

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

Principal Investigator

MONKAWA Toshiaki  慶應義塾大学, 医学部, 教授 (80286484)

Project Period (FY) 2012-04-01 – 2015-03-31
Keywords腎臓 / 尿細管 / ES細胞 / iPS細胞 / miRNA
Outline of Final Research Achievements

We developed a method of inducing renal tubular cells from mouse embryonic stem cells via the cell purification of kidney specific protein (KSP)-positive cells using an anti-KSP antibody. KSP-positive cells had the capacity to form tubular structures when grown in a 3D culture in Matrigel. Moreover, KSP-positive cells acquired the characteristics of each segment of renal tubular cells through tubular formation when stimulated with Wnt4. Human ES cells were not willing to differentiate into tubular cells compared to mouse ES cells. GSK-3β-inhibitor increased KSP-positive cells.
We examined miRNA expression in experimental models of EMT and renal epithelialization using microarray, and found that miR-34c attenuates EMT induced by TGF-β in a mouse tubular cell line. To confirm the effects of miR-34c in vivo, we administered the precursor of miR-34c to mice with unilateral ureteral obstruction, and miR-34c decreased kidney fibrosis.

Free Research Field

腎臓内科学

URL: 

Published: 2016-06-03  

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