SEARCH:   Advanced

Blood, 1 September 2006, Vol. 108, No. 5, pp. 1758-1766. Prepublished online as a Blood First Edition Paper on May 18, 2006; DOI 10.1182/blood-2006-05-021881. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-05-021881v1 108/5/1758    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 Hazan-Eitan, Z. Articles by Levy, R. Search for Related Content PubMed PubMed Citation Articles by Hazan-Eitan, Z. Articles by Levy, R. Related Collections Immunobiology Phagocytes Signal Transduction Gene Expression Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  PHAGOCYTES Induction of FcRIIA expression in myeloid PLB cells during differentiation depends on cytosolic phospholipase A2 activity and is regulated via activation of CREB by PGE2 Zahit Hazan-Eitan, Yacob Weinstein, Nurit Hadad, Aviva Konforty, and Rachel Levy From the Infectious Diseases Laboratory, Department of Clinical Biochemistry and Department of Microbiology and Immunology, Faculty of Health Sciences, Ben-Gurion University of the Negev and Soroka Medical Center, Beer Sheva, Israel. FcRIIA expressed on neutrophils and monocytes has a fundamental role in combating bacterial infections. In the present study, the requirement of cytosolic phospholipase A2 (cPLA2) for induction of FcRIIA expression was studied in a model of cPLA2-deficient PLB-985 cells (PLB-D cells). FcRIIA was acquired only during differentiation of PLB but not of PLB-D cells induced by either 1,25-dihydroxyvitamin D3, retinoic acid, or interferon . Addition of prostaglandin E2 (PGE2) to PLB-D cells undergoing differentiation restored the expression of FcRIIA protein, whereas addition of indomethacin to PLB cells during differentiation inhibited both the production of PGE2 and the expression of FcRIIA. Inhibition of PKA during PLB differentiation prevented FcRIIA expression, whereas dibutyryl cAMP (dbcAMP) induced its expression in both PLB and PLB-D cells. CREB phosphorylation and CREB-CRE interaction were detected only in differentiated PLB cells and not PLB-D cells and were inhibited by indomethacin. A reporter gene containing a FcRIIA gene promoter fragment with the CRE element was sufficient for CREB activation. Our results are the first to show that CREB activation is involved in up-regulation of FcRIIA expression in myeloid lineages. PGE2 formed via cPLA2 activates CREB through PKA and this process is dependent on development of PGE2 receptor 4. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. H. Serezani, M. N. Ballinger, D. M. Aronoff, and M. Peters-Golden Cyclic AMP: Master Regulator of Innate Immune Cell Function Am. J. Respir. Cell Mol. Biol., August 1, 2008; 39(2): 127 - 132. [Abstract] [Full Text] [PDF] T. Khayrullina, J.-H. Yen, H. Jing, and D. Ganea In Vitro Differentiation of Dendritic Cells in the Presence of Prostaglandin E2 Alters the IL-12/IL-23 Balance and Promotes Differentiation of Th17 Cells J. Immunol., July 1, 2008; 181(1): 721 - 735. [Abstract] [Full Text] [PDF]

	Copyright © 2006 by American Society of Hematology         Online ISSN: 1528-0020