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 Blood, 25 June 2009, Vol. 113, No. 26, pp. 6699-6706.
Prepublished online as a Blood First Edition Paper on April 24, 2009; DOI 10.1182/blood-2008-11-186312.

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PLATELETS AND THROMBOPOIESIS

PAF-acetylhydrolase expressed during megakaryocyte differentiation inactivates PAF-like lipids

Jason M. Foulks1,2, Gopal K. Marathe3, Noemi Michetti2, Diana M. Stafforini4,5, Guy A. Zimmerman2,4, Thomas M. McIntyre3, and Andrew S. Weyrich2,4

1 Department of Experimental Pathology, and 2 Program in Human Molecular Biology and Genetics, University of Utah, Salt Lake City; 3 Department of Cell Biology, Lerner Research Institute, The Cleveland Clinic, OH; and 4 Department of Internal Medicine, and 5 Huntsman Cancer Institute, University of Utah, Salt Lake City

Platelet activating factor (PAF) and PAF-like lipids induce inflammatory responses in target cells. These lipid mediators are inactivated by PAF-acetylhydrolase (PAF-AH). The PAF signaling system affects the growth of hematopoietic CD34+ cells, but roles for PAF-AH in this process are unknown. Here, we investigated PAF-AH function during megakaryopoiesis and found that human CD34+ cells accumulate this enzymatic activity as they differentiate toward megakaryocytes, consistent with the expression of mRNA and protein for the plasma PAF-AH isoform. Inhibition of endogenous PAF-AH activity in differentiated megakaryocytes increased formation of lipid mediators that signaled the PAF receptor (PAFR) in fully differentiated human cells such as neutrophils, as well as megakaryocytes themselves. PAF-AH also controlled megakaryocyte {alpha}IIbβ3-dependent adhesion, cell spreading, and mobility that relied on signaling through the PAFR. Together these data suggest that megakaryocytes generate PAF-AH to modulate the accumulation of intracellular phospholipid mediators that may detrimentally affect megakaryocyte development and function.


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