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

(2015) PLOS ONE. 10(2).
Author
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Abstract
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.
Keywords
CELL-MIGRATION, ALTERNATIVE ACTIVATION, KIDNEY PROXIMAL TUBULE, NITRIC-OXIDE SYNTHASE, PHOSPHOINOSITIDE 3-KINASE, PERITONEAL-DIALYSIS, J774 MACROPHAGES, PHOSPHOLIPASE-C, LEADING-EDGE, MDCK CELLS

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Citation

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MLA
Tyteca, Donatienne et al. “Regulation of Macrophage Motility by the Water Channel Aquaporin-1 : Crucial Role of M0/M2 Phenotype Switch.” PLOS ONE 10.2 (2015): n. pag. Print.
APA
Tyteca, D., Nishino, T., Debaix, H., Van Der Smissen, P., N’Kuli, F., Hoffmann, D., Cnops, Y., et al. (2015). Regulation of macrophage motility by the water channel aquaporin-1 : crucial role of M0/M2 phenotype switch. PLOS ONE, 10(2).
Chicago author-date
Tyteca, Donatienne, Tomoya Nishino, Huguette Debaix, Patrick Van Der Smissen, Francisca N’Kuli, Delia Hoffmann, Yvette Cnops, et al. 2015. “Regulation of Macrophage Motility by the Water Channel Aquaporin-1 : Crucial Role of M0/M2 Phenotype Switch.” Plos One 10 (2).
Chicago author-date (all authors)
Tyteca, Donatienne, 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, and Pierre J Courtoy. 2015. “Regulation of Macrophage Motility by the Water Channel Aquaporin-1 : Crucial Role of M0/M2 Phenotype Switch.” Plos One 10 (2).
Vancouver
1.
Tyteca D, Nishino T, Debaix H, Van Der Smissen P, N’Kuli F, Hoffmann D, et al. Regulation of macrophage motility by the water channel aquaporin-1 : crucial role of M0/M2 phenotype switch. PLOS ONE. 2015;10(2).
IEEE
[1]
D. Tyteca et al., “Regulation of macrophage motility by the water channel aquaporin-1 : crucial role of M0/M2 phenotype switch,” PLOS ONE, vol. 10, no. 2, 2015.
@article{5930103,
  abstract     = {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.},
  articleno    = {e0117398},
  author       = {Tyteca, Donatienne and Nishino, Tomoya and Debaix, Huguette and Van Der Smissen, Patrick and N'Kuli, Francisca and Hoffmann, Delia and Cnops, Yvette and Rabolli, Virginie and van Loo, Geert and Beyaert, Rudi and Huaux, François and Devuyst, Olivier and Courtoy, Pierre J},
  issn         = {1932-6203},
  journal      = {PLOS ONE},
  keywords     = {CELL-MIGRATION,ALTERNATIVE ACTIVATION,KIDNEY PROXIMAL TUBULE,NITRIC-OXIDE SYNTHASE,PHOSPHOINOSITIDE 3-KINASE,PERITONEAL-DIALYSIS,J774 MACROPHAGES,PHOSPHOLIPASE-C,LEADING-EDGE,MDCK CELLS},
  language     = {eng},
  number       = {2},
  pages        = {23},
  title        = {Regulation of macrophage motility by the water channel aquaporin-1 : crucial role of M0/M2 phenotype switch},
  url          = {http://dx.doi.org/10.1371/journal.pone.0117398},
  volume       = {10},
  year         = {2015},
}

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