LysoPC and PAF Trigger Arachidonic Acid Release by Divergent Signaling Mechanisms in MonocytesReport as inadecuate




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Journal of LipidsVolume 2011 2011, Article ID 532145, 11 pages

Research Article

Department of Biology, Norwegian University of Science and Technology, 7491 Trondheim, Norway

Faculty of Medicine, Norwegian University of Science and Technology, 7491 Trondheim, Norway

Section for Biotechnology, Molecular, and Environmental Biology, Department of Biology, Norwegian University of Science and Technology, 7491 Trondheim, Norway

Received 17 March 2011; Revised 29 April 2011; Accepted 28 May 2011

Academic Editor: Angeliki Chroni

Copyright © 2011 Janne Oestvang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Oxidized low-density lipoproteins LDLs play an important role during the development of atherosclerosis characterized by intimal inflammation and macrophage accumulation. A key component of LDL is lysophosphatidylcholine lysoPC. LysoPC is a strong proinflammatory mediator, and its mechanism is uncertain, but it has been suggested to be mediated via the platelet activating factor PAF receptor. Here, we report that PAF triggers a pertussis toxin- PTX- sensitive intracellular signaling pathway leading to sequential activation of sPLA2, PLD, cPLA2, and AA release in human-derived monocytes. In contrast, lysoPC initiates two signaling pathways, one sequentially activating PLD and cPLA2, and a second parallel PTX-sensitive pathway activating cPLA2 with concomitant activation of sPLA2, all leading to AA release. In conclusion, lysoPC and PAF stimulate AA release by divergent pathways suggesting involvement of independent receptors. Elucidation of monocyte lysoPC-specific signaling mechanisms will aid in the development of novel strategies for atherosclerosis prevention, diagnosis, and therapy.





Author: Janne Oestvang, Marit W. Anthonsen, and Berit Johansen

Source: https://www.hindawi.com/



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