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Prepublished online as a Blood First Edition Paper on May 22, 2003; DOI 10.1182/blood-2002-09-2936. This Article Full Text (PDF) Supplemental Figures All Versions of this Article: 2002-09-2936v1 102/6/2251    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 Chodniewicz, D. Articles by Zhelev, D. V Search for Related Content PubMed PubMed Citation Articles by Chodniewicz, D. Articles by Zhelev, D. V Social Bookmarking                   What's this? Submitted September 26, 2002 Accepted May 6, 2003 Novel pathways of F-actin polymerization in the human neutrophil David Chodniewicz and Doncho V Zhelev* Department of Mechanical Engineering and Materials Science, Duke University, Durham, NC, USA * Corresponding author; email: dvzh{at}duke.edu. Recently we demonstrated the existence of a PI3K-independent F-actin polymerization during neutrophil pseudopod extension. Here we examine the utilization of the PI3K-dependent and -independent pathways of activation by the N-formyl peptide receptor and the chemokine receptors, and the priming of the two pathways by GM-CSF and insulin. The inhibition of PI3K activity with wortmannin showed that rate of pseudopod extension stimulated with fMLP was mostly dependent on PI3K, while the rate of IL-8-stimulated pseudopod extension was less dependent on PI3K. The incubation of cells with either GM-CSF or insulin increased the rate of pseudopod extension by 50% when the cells were stimulated with IL-8 but not fMLP. The stimulation with IL-8 phosphorylated the PI3K regulatory subunit. This phosphorylation was enhanced by GM-CSF, which increased PI3K activity and total PtdIns(3,4,5)P3 production. The effect of GM-CSF was blocked with wortmannin. In contrast, insulin did not increase p85 phosphorylation and did not enhance PI3K activity or PtdIns(3,4,5)P3 production. The effect of insulin was insensitive to wortmannin, however it was blocked by an SH2-binding peptide. These data indicate that priming of IL-8 activation with GM-CSF was mediated via the PI3Ks of class IA, while priming with insulin used a PI3K-independent pathway. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. McArthur, S. Yazid, H. Christian, R. Sirha, R. Flower, J. Buckingham, and E. Solito Annexin A1 regulates hormone exocytosis through a mechanism involving actin reorganization FASEB J, November 1, 2009; 23(11): 4000 - 4010. [Abstract] [Full Text] [PDF] B. Heit, L. Liu, P. Colarusso, K. D. Puri, and P. Kubes PI3K accelerates, but is not required for, neutrophil chemotaxis to fMLP J. Cell Sci., January 15, 2008; 121(2): 205 - 214. [Abstract] [Full Text] [PDF] M. A. Sanjuan, N. Rao, K.-T. A. Lai, Y. Gu, S. Sun, A. Fuchs, W.-P. Fung-Leung, M. Colonna, and L. Karlsson CpG-induced tyrosine phosphorylation occurs via a TLR9-independent mechanism and is required for cytokine secretion. J. Cell Biol., March 27, 2006; 172(7): 1057 - 1068. [Abstract] [Full Text] [PDF] X. Jiao, N. Zhang, X. Xu, J. J. Oppenheim, and T. Jin Ligand-Induced Partitioning of Human CXCR1 Chemokine Receptors with Lipid Raft Microenvironments Facilitates G-Protein-Dependent Signaling Mol. Cell. Biol., July 1, 2005; 25(13): 5752 - 5762. [Abstract] [Full Text] [PDF] L. Riol-Blanco, N. Sanchez-Sanchez, A. Torres, A. Tejedor, S. Narumiya, A. L. Corbi, P. Sanchez-Mateos, and J. L. Rodriguez-Fernandez The Chemokine Receptor CCR7 Activates in Dendritic Cells Two Signaling Modules That Independently Regulate Chemotaxis and Migratory Speed J. Immunol., April 1, 2005; 174(7): 4070 - 4080. [Abstract] [Full Text] [PDF] G. M. Fuhler, G. J. Knol, A. L. Drayer, and E. Vellenga Impaired interleukin-8- and GRO{alpha}-induced phosphorylation of extracellular signal-regulated kinase result in decreased migration of neutrophils from patients with myelodysplasia J. Leukoc. Biol., February 1, 2005; 77(2): 257 - 266. [Abstract] [Full Text] [PDF] P. J. Barnes Mediators of Chronic Obstructive Pulmonary Disease Pharmacol. Rev., December 1, 2004; 56(4): 515 - 548. [Abstract] [Full Text] [PDF] D. Chodniewicz, A. M. Alteraifi, and D. V. Zhelev Experimental Evidence for the Limiting Role of Enzymatic Reactions in Chemoattractant-induced Pseudopod Extension in Human Neutrophils J. Biol. Chem., June 4, 2004; 279(23): 24460 - 24466. [Abstract] [Full Text] [PDF]

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