ARP3 Controls the Podocyte Architecture at the Kidney Filtration Barrier
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ARP3 Controls the Podocyte Architecture at the Kidney Filtration Barrier. / Schell, Christoph; Sabass, Benedikt; Helmstaedter, Martin; Geist, Felix; Abed, Ahmed; Yasuda-Yamahara, Mako; Sigle, August; Maier, Jasmin I; Grahammer, Florian; Siegerist, Florian; Artelt, Nadine; Endlich, Nicole; Kerjaschki, Dontscho; Arnold, Hans-Henning; Dengjel, Jörn; Rogg, Manuel; Huber, Tobias B.
in: DEV CELL, Jahrgang 47, Nr. 6, 17.12.2018, S. 741-757.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - ARP3 Controls the Podocyte Architecture at the Kidney Filtration Barrier
AU - Schell, Christoph
AU - Sabass, Benedikt
AU - Helmstaedter, Martin
AU - Geist, Felix
AU - Abed, Ahmed
AU - Yasuda-Yamahara, Mako
AU - Sigle, August
AU - Maier, Jasmin I
AU - Grahammer, Florian
AU - Siegerist, Florian
AU - Artelt, Nadine
AU - Endlich, Nicole
AU - Kerjaschki, Dontscho
AU - Arnold, Hans-Henning
AU - Dengjel, Jörn
AU - Rogg, Manuel
AU - Huber, Tobias B
N1 - Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.
PY - 2018/12/17
Y1 - 2018/12/17
N2 - Podocytes, highly specialized epithelial cells, build the outer part of the kidney filtration barrier and withstand high mechanical forces through a complex network of cellular protrusions. Here, we show that Arp2/3-dependent actin polymerization controls actomyosin contractility and focal adhesion maturation of podocyte protrusions and thereby regulates formation, maintenance, and capacity to adapt to mechanical requirements of the filtration barrier. We find that N-WASP-Arp2/3 define the development of complex arborized podocyte protrusions in vitro and in vivo. Loss of dendritic actin networks results in a pronounced activation of the actomyosin cytoskeleton and the generation of over-maturated but less efficient adhesion, leading to detachment of podocytes. Our data provide a model to explain podocyte protrusion morphology and their mechanical stability based on a tripartite relationship between actin polymerization, contractility, and adhesion.
AB - Podocytes, highly specialized epithelial cells, build the outer part of the kidney filtration barrier and withstand high mechanical forces through a complex network of cellular protrusions. Here, we show that Arp2/3-dependent actin polymerization controls actomyosin contractility and focal adhesion maturation of podocyte protrusions and thereby regulates formation, maintenance, and capacity to adapt to mechanical requirements of the filtration barrier. We find that N-WASP-Arp2/3 define the development of complex arborized podocyte protrusions in vitro and in vivo. Loss of dendritic actin networks results in a pronounced activation of the actomyosin cytoskeleton and the generation of over-maturated but less efficient adhesion, leading to detachment of podocytes. Our data provide a model to explain podocyte protrusion morphology and their mechanical stability based on a tripartite relationship between actin polymerization, contractility, and adhesion.
KW - Journal Article
U2 - 10.1016/j.devcel.2018.11.011
DO - 10.1016/j.devcel.2018.11.011
M3 - SCORING: Journal article
C2 - 30503751
VL - 47
SP - 741
EP - 757
JO - DEV CELL
JF - DEV CELL
SN - 1534-5807
IS - 6
ER -