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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.
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PHAGOCYTES
Induction of Fc RIIA 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.
Fc RIIA 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.
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