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Título

Cyclooxygenase-2 deficiency in macrophages leads to defective p110γ PI3K signaling and impairs cell, adhesion and migration

Autor Díaz-Muñoz, Manuel D.; Osma-García, Inés C.; Íñiguez, Miguel Ángel ; Fresno, Manuel
Fecha de publicación 2013
EditorAmerican Association of Immunologists
Citación Journal of Immunology 191: 395- 406 (2013)
ResumenCyclooxygenase (Cox)-2 dependent PGs modulate several functions in many pathophysiological processes, including migration of immune cells. In this study, we addressed the role of Cox-2 in macrophage migration by using in vivo and in vitro models. Upon thioglycolate challenge, CD11b+ F4/80 + macrophages showed a diminished ability to migrate to the peritoneal cavity in cox-2-/- mice. In vivo migration of cox-2 -/- macrophages from the peritoneal cavity to lymph nodes, as well as cell adhesion to the mesothelium, was reduced in response to LPS. In vitro migration of cox-2-/- macrophages toward MCP-1, RANTES, MIP-1α, or MIP-1β, as well as cell adhesion to ICAM-1 or fibronectin, was impaired. Defects in cell migration were not due to changes in chemokine receptor expression. Remarkably, cox-2-/- macrophages showed a deficiency in focal adhesion formation, with reduced phosphorylation of paxillin (Tyr188). Interestingly, expression of the p110γ catalytic subunit of PI3K was severely reduced in the absence of Cox-2, leading to defective Akt phosphorylation, as well as cdc42 and Rac-1 activation. Our results indicate that the paxillin/p110γ-PI3K/Cdc42/Rac1 axis is defective in cox-2-/- macrophages, which results in impaired cell adhesion and migration. Copyright © 2013 by The American Association.
URI http://hdl.handle.net/10261/95733
DOI10.4049/jimmunol.1202002
Identificadoresdoi: 10.4049/jimmunol.1202002
issn: 0022-1767
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