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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 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 Citation Map 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. Related Collections Phagocytes Cytoskeleton Signal Transduction Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 September 2003, Vol. 102, No. 6, pp. 2251-2258 PHAGOCYTES Novel pathways of F-actin polymerization in the human neutrophil David Chodniewicz, and Doncho V. Zhelev From the Department of Mechanical Engineering and Materials Science, Duke University, Durham, NC. Recently we demonstrated the existence of a phosphatidylinositol 3-kinase (PI3K)–independent F-actin polymerization during neutrophil pseudopod extension. Here we examine the use of the PI3K-dependent and PI3K-independent pathways of activation by the N-formyl peptide receptor and the chemokine receptors, and the priming of the 2 pathways by granulocyte-macrophage colony-stimulating factor (GM-CSF) and insulin. The inhibition of PI3K activity with wortmannin showed that rate of pseudopod extension stimulated with N-formyl-Met-Leu-Phe (fMLP was mostly dependent on PI3K, while the rate of interleukin-8 (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 with fMLP. The stimulation with IL-8 phosphorylated the PI3K regulatory subunit. This phosphorylation was enhanced by GM-CSF, which increased PI3K activity and total phosphatidylinositol 3,4,5-trisphosphate (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 Src homology 2 (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: 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. 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Rev., December 1, 2004; 56(4): 515 - 548. [Abstract] [Full Text] [PDF] D. V. Zhelev, A. M. Alteraifi, and D. Chodniewicz Controlled Pseudopod Extension of Human Neutrophils Stimulated with Different Chemoattractants Biophys. J., July 1, 2004; 87(1): 688 - 695. [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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