Arachidonic acid metabolism by human monocytes. Studies with platelet- depleted cultures

doi:10.1084/jem.158.2.393

This Article

	Full Text (PDF, 1620K)
	Alert me when this article is cited
	Citation Map

Services

	Email this article
	Similar articles in this journal
	Similar articles in PubMed
	Alert me to new content in the JEM
	Download to citation manager

Citing Articles

	Citing Articles via HighWire
	Citing Articles via CrossRef
	Citing Articles via Google Scholar

Google Scholar

	Articles by Pawlowski, N. A.
	Articles by Scott, W. A.
	Search for Related Content

PubMed

	PubMed Citation
	Articles by Pawlowski, N. A.
	Articles by Scott, W. A.


Social Bookmarking

	What's this?

ARTICLES

Arachidonic acid metabolism by human monocytes. Studies with platelet- depleted cultures

NA Pawlowski, G Kaplan, AL Hamill, ZA Cohn and WA Scott

Purified human monocytes release and metabolize endogenous arachidonic acid (20:4) from phospholipid stores when challenged with particulate inflammatory stimuli or the calcium ionophore A23187. Using radiolabeled cultures, the percentage of total [3H]20:4 released was similar with each type of stimulus. However, the spectrum of 20:4 metabolites differed. With opsonized zymosan (OpZ) or Sephadex beads coated with IgG immune complexes (Ig-beads), the predominant product was thromboxane (25% of the total) together with smaller amounts of other cyclo-oxygenase products and lipoxygenase metabolites. Levels of thromboxane synthesis by monocytes were comparable to those by platelets, as measured by radioimmunoassay. In contrast, exposure to the nonspecific agent A23187 led to mainly lipoxygenase products (70% of the total). Monocytes isolated from mononuclear cell fractions of peripheral blood contain platelets specifically rosetted to their surfaces. These platelet contaminants were removed by sequential incubations of monocytes in serum and EDTA followed by adherence and detachment from tissue culture vessels. The presence of platelets in routinely isolated monocytes presented a major difficulty in the study of human monocyte 20:4 metabolism since platelets also synthesize thromboxane. Loss of 12-HETE synthesis (16-fold reduction relative to 5- HETE) in A23187-stimulated cultures provided a convenient measure of platelet depletion. This together with the response to monocyte- specific stimuli (OpZ and Ig-beads) allowed for the distinction between monocyte and platelet 20:4 metabolism.
Add to CiteULike CiteULike Add to Complore Complore Add to Connotea Connotea Add to Del.icio.us Del.icio.us Add to Digg Digg Facebook Add to Reddit Reddit Add to Technorati Technorati Twitter What's this?

This article has been cited by other articles:

Wygrecka, M., Marsh, L. M., Morty, R. E., Henneke, I., Guenther, A., Lohmeyer, J., Markart, P., Preissner, K. T. (2009). Enolase-1 promotes plasminogen-mediated recruitment of monocytes to the acutely inflamed lung. Blood 113: 5588-5598 [Abstract] [Full Text]
Patel, P., Cossette, C., Anumolu, J. R., Erlemann, K.-R., Grant, G. E., Rokach, J., Powell, W. S. (2009). Substrate Selectivity of 5-Hydroxyeicosanoid Dehydrogenase and Its Inhibition by 5-Hydroxy-{Delta}6-Long-Chain Fatty Acids. J. Pharmacol. Exp. Ther. 329: 335-341 [Abstract] [Full Text]
McAdam, B. F., Byrne, D., Morrow, J. D., Oates, J. A. (2005). Contribution of Cyclooxygenase-2 to Elevated Biosynthesis of Thromboxane A2 and Prostacyclin in Cigarette Smokers. Circulation 112: 1024-1029 [Abstract] [Full Text]
OSTERUD, B., BJORKLID, E. (2003). Role of Monocytes in Atherogenesis. Physiol. Rev. 83: 1069-1112 [Abstract] [Full Text]
Hattar, K., Bickenbach, A., Csernok, E., Rosseau, S., Grandel, U., Seeger, W., Grimminger, F., Sibelius, U. (2002). Wegener's granulomatosis: antiproteinase 3 antibodies induce monocyte cytokine and prostanoid release--role of autocrine cell activation. J. Leukoc. Biol. 71: 996-1004 [Abstract] [Full Text]
Penglis, P. S., Cleland, L. G., Demasi, M., Caughey, G. E., James, M. J. (2000). Differential Regulation of Prostaglandin E2 and Thromboxane A2 Production in Human Monocytes: Implications for the Use of Cyclooxygenase Inhibitors. J. Immunol. 165: 1605-1611 [Abstract] [Full Text]
Yoshida, K., Ono, M., Sawada, H. (1999). Lipopolysaccharide-induced vacuoles in macrophages: Their origin is plasma membrane-derived organelles and endoplasmic reticulum, but not lysosomes. Innate Immunity 5: 127-137 [Abstract]
Klouche, M., May, A. E., Hemmes, M., Me�ner, M., Kanse, S. M., Preissner, K. T., Bhakdi, S. (1999). Enzymatically Modified, Nonoxidized LDL Induces Selective Adhesion and Transmigration of Monocytes and T-Lymphocytes Through Human Endothelial Cell Monolayers. Arterioscler. Thromb. Vasc. Bio. 19: 784-793 [Abstract] [Full Text]
Locati, M., Lamorte, G., Luini, W., Introna, M., Bernasconi, S., Mantovani, A., Sozzani, S. (1996). Inhibition of Monocyte Chemotaxis to C-C Chemokines by Antisense Oligonucleotide for Cytosolic Phospholipase A(2). J. Biol. Chem. 271: 6010-6016 [Abstract] [Full Text]