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...
| প্রধান লেখক: | , , , , , , , , , , , , |
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| বিন্যাস: | প্রবন্ধ |
| ভাষা: | English |
| প্রকাশিত: |
Public Library of Science (PLoS)
2015-01-01
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| মালা: | PLoS ONE |
| অনলাইন ব্যবহার করুন: | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0117398&type=printable |
| _version_ | 1826586609210884096 |
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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. |
| first_indexed | 2024-04-11T20:17:12Z |
| format | Article |
| id | doaj.art-945a74e25259425f9875a968419b6d35 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2025-03-14T16:12:15Z |
| publishDate | 2015-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-945a74e25259425f9875a968419b6d352025-02-23T05:31:58ZengPublic 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://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0117398&type=printable |
| 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://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0117398&type=printable |
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