Regulation of macrophage motility by the water channel aquaporin-1: crucial role of M0/M2 phenotype switch.

The water channel aquaporin-1 (AQP1) promotes migration of many cell types. Although AQP1 is expressed in macrophages, its potential role in macrophage motility, particularly in relation with phenotype polarization, remains unknown. We here addressed these issues in peritoneal macrophages isolated f...

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Main Authors: Donatienne Tyteca, Tomoya Nishino, Huguette Debaix, Patrick Van Der Smissen, Francisca N'Kuli, Delia Hoffmann, Yvette Cnops, Virginie Rabolli, Geert van Loo, Rudi Beyaert, François Huaux, Olivier Devuyst, Pierre J Courtoy
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2015-01-01
Series:PLoS ONE
Online Access:https://doi.org/10.1371/journal.pone.0117398
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author Donatienne Tyteca
Tomoya Nishino
Huguette Debaix
Patrick Van Der Smissen
Francisca N'Kuli
Delia Hoffmann
Yvette Cnops
Virginie Rabolli
Geert van Loo
Rudi Beyaert
François Huaux
Olivier Devuyst
Pierre J Courtoy
author_facet Donatienne Tyteca
Tomoya Nishino
Huguette Debaix
Patrick Van Der Smissen
Francisca N'Kuli
Delia Hoffmann
Yvette Cnops
Virginie Rabolli
Geert van Loo
Rudi Beyaert
François Huaux
Olivier Devuyst
Pierre J Courtoy
author_sort Donatienne Tyteca
collection DOAJ
description The water channel aquaporin-1 (AQP1) promotes migration of many cell types. Although AQP1 is expressed in macrophages, its potential role in macrophage motility, particularly in relation with phenotype polarization, remains unknown. We here addressed these issues in peritoneal macrophages isolated from AQP1-deficient mice, either undifferentiated (M0) or stimulated with LPS to orientate towards pro-inflammatory phenotype (classical macrophage activation; M1). In non-stimulated macrophages, ablation of AQP1 (like inhibition by HgCl2) increased by 2-3 fold spontaneous migration in a Src/PI3K/Rac-dependent manner. This correlated with cell elongation and formation of lamellipodia/ruffles, resulting in membrane lipid and F4/80 recruitment to the leading edge. This indicated that AQP1 normally suppresses migration of resting macrophages, as opposed to other cell types. Resting Aqp1-/- macrophages exhibited CD206 redistribution into ruffles and increased arginase activity like IL4/IL13 (alternative macrophage activation; M2), indicating a M0-M2 shift. In contrast, upon M1 orientation by LPS in vitro or peritoneal inflammation in vivo, migration of Aqp1-/- macrophages was reduced. Taken together, these data indicate that AQP1 oppositely regulates macrophage migration, depending on stimulation or not by LPS, and that macrophage phenotypic and migratory changes may be regulated independently of external cues.
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spelling doaj.art-945a74e25259425f9875a968419b6d352022-12-22T04:04:55ZengPublic Library of Science (PLoS)PLoS ONE1932-62032015-01-01102e011739810.1371/journal.pone.0117398Regulation of macrophage motility by the water channel aquaporin-1: crucial role of M0/M2 phenotype switch.Donatienne TytecaTomoya NishinoHuguette DebaixPatrick Van Der SmissenFrancisca N'KuliDelia HoffmannYvette CnopsVirginie RabolliGeert van LooRudi BeyaertFrançois HuauxOlivier DevuystPierre J CourtoyThe water channel aquaporin-1 (AQP1) promotes migration of many cell types. Although AQP1 is expressed in macrophages, its potential role in macrophage motility, particularly in relation with phenotype polarization, remains unknown. We here addressed these issues in peritoneal macrophages isolated from AQP1-deficient mice, either undifferentiated (M0) or stimulated with LPS to orientate towards pro-inflammatory phenotype (classical macrophage activation; M1). In non-stimulated macrophages, ablation of AQP1 (like inhibition by HgCl2) increased by 2-3 fold spontaneous migration in a Src/PI3K/Rac-dependent manner. This correlated with cell elongation and formation of lamellipodia/ruffles, resulting in membrane lipid and F4/80 recruitment to the leading edge. This indicated that AQP1 normally suppresses migration of resting macrophages, as opposed to other cell types. Resting Aqp1-/- macrophages exhibited CD206 redistribution into ruffles and increased arginase activity like IL4/IL13 (alternative macrophage activation; M2), indicating a M0-M2 shift. In contrast, upon M1 orientation by LPS in vitro or peritoneal inflammation in vivo, migration of Aqp1-/- macrophages was reduced. Taken together, these data indicate that AQP1 oppositely regulates macrophage migration, depending on stimulation or not by LPS, and that macrophage phenotypic and migratory changes may be regulated independently of external cues.https://doi.org/10.1371/journal.pone.0117398
spellingShingle Donatienne Tyteca
Tomoya Nishino
Huguette Debaix
Patrick Van Der Smissen
Francisca N'Kuli
Delia Hoffmann
Yvette Cnops
Virginie Rabolli
Geert van Loo
Rudi Beyaert
François Huaux
Olivier Devuyst
Pierre J Courtoy
Regulation of macrophage motility by the water channel aquaporin-1: crucial role of M0/M2 phenotype switch.
PLoS ONE
title Regulation of macrophage motility by the water channel aquaporin-1: crucial role of M0/M2 phenotype switch.
title_full Regulation of macrophage motility by the water channel aquaporin-1: crucial role of M0/M2 phenotype switch.
title_fullStr Regulation of macrophage motility by the water channel aquaporin-1: crucial role of M0/M2 phenotype switch.
title_full_unstemmed Regulation of macrophage motility by the water channel aquaporin-1: crucial role of M0/M2 phenotype switch.
title_short Regulation of macrophage motility by the water channel aquaporin-1: crucial role of M0/M2 phenotype switch.
title_sort regulation of macrophage motility by the water channel aquaporin 1 crucial role of m0 m2 phenotype switch
url https://doi.org/10.1371/journal.pone.0117398
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