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Blood, 1 February 2007, Vol. 109, No. 3, pp. 1257-1264. Prepublished online as a Blood First Edition Paper on September 21, 2006; DOI 10.1182/blood-2006-04-017731. This Article Full Text (PDF) All Versions of this Article: blood-2006-04-017731v1 109/3/1257    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Filippi, M.-D. Articles by Berclaz, P.-Y. Search for Related Content PubMed PubMed Citation Articles by Filippi, M.-D. Articles by Berclaz, P.-Y. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted April 17, 2006 Accepted September 6, 2006 The Rho GTPase Rac1 is critical for neutrophil migration into the lung Marie-Dominique Filippi*, Kathleen Szczur, Chad Harris, and Pierre-Yves Berclaz Division Experimental Hematology, University of Cincinnati College of Medicine, Cincinnati, OH Division Pulmonary Medicine, University of Cincinnati College of Medicine, Cincinnati, OH * Corresponding author; email: marie-dominique.filippi{at}cchmc.org. Neutrophils are critical in the inflammatory process by moving rapidly to tissue sites of inflammation. Members of the small Rho GTPase family, Rac1, Rac2, CDC42 and RhoA, are central regulators of cell migration via cytoskeleton rearrangement. The role of Rac1 in neutrophil migration related to inflammatory processes has remained elusive and has yet to be determined in physiological in vivo models. We previously demonstrated a role for Rac1 in tail retraction (Gu, et al, Science, 2003). Here, we present evidence that Rac1-mediated uropod formation may be due to cross talk with a related Rho GTPase RhoA. To assess the physiological relevance of these findings, we utilized adoptive transfer of Rac1flox/flox bone marrow cells which allows post-engraftment in vivo deletion of Rac1 only in blood cells. We examined the specific role of Rac1 in neutrophil migration into the lung during the inflammatory process induced by formyl-methionyl-leucyl-phenylalanine exposure. The loss of Rac1 activity in neutrophils is associated with a significant decreased neutrophil recruitment into lung alveolar and attenuation of emphysematous lesions. Overall, this study suggests that Rac1 is a physiological integrator of signals for neutrophil recruitment into lung tissue during an inflammatory response. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: K. Szczur, Y. Zheng, and M.-D. Filippi The small Rho GTPase Cdc42 regulates neutrophil polarity via CD11b integrin signaling Blood, November 12, 2009; 114(20): 4527 - 4537. [Abstract] [Full Text] [PDF] A. K. Azab, F. Azab, S. Blotta, C. M. Pitsillides, B. Thompson, J. M. Runnels, A. M. Roccaro, H. T. Ngo, M. R. Melhem, A. Sacco, et al. RhoA and Rac1 GTPases play major and differential roles in stromal cell-derived factor-1-induced cell adhesion and chemotaxis in multiple myeloma Blood, July 16, 2009; 114(3): 619 - 629. [Abstract] [Full Text] [PDF] R. A. Lacalle, R. M. Peregil, J. P. Albar, E. Merino, C. Martinez-A, I. Merida, and S. Manes Type I phosphatidylinositol 4-phosphate 5-kinase controls neutrophil polarity and directional movement J. Cell Biol., December 31, 2007; 179(7): 1539 - 1553. [Abstract] [Full Text] [PDF]

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