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      15-oxoeicosatetraenoic acid mediates monocyte adhesion to endothelial cell

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          Abstract

          Background

          A great number of studies reported that 12/15-lipoxygenase (12/15-LO) played an important role in atherosclerosis. And its arachidonic acid(AA) metabolite, 15(S)-hydroperoxy-5,8,11,13-(Z,Z,Z,E)-eicosatetraenoic acid (15(S)-HETE), is demonstrated to mediate endothelial dysfunction. 15-oxo-5,8,11,13-(Z,Z,Z,E)-eicosatetraenoic acid (15-oxo-ETE) was formed from 15-hydroxyprostaglandin dehydrogenase (PGDH)-mediated oxidation of 15(S)-HETE. However, relatively little is known about the biological effects of 15-oxo-ETE in cardiovascular disease. Here, we explore the likely role of 15-lipoxygenase (LO)-1-mediated AA metabolism,15-oxo-ETE, in the early pathogenesis of atherosclerosis.

          Methods

          The 15-oxo-ETE level in serum was detected by means of liquid chromatography and online tandem mass spectrometry (LC-MS/MS). And the underlying mechanisms were illuminated by molecular techniques, including immunoblotting, MTT assay, immunocytochemistry and Immunohistochemistry.

          Results

          Increased 15-oxo-ETE level is found in in patients with acute myocardial infarction (AMI). After 15-oxo-ETE treatment, Human umbilical vein endothelial cells (HUVECs) showed more attractive to monocytes, whereas monocyte adhesion is suppressed when treated with PKC inhibitor. In ex vivo study, exposure of arteries from C57 mice and ApoE−/−mice to 15-oxo-ETE led to significantly increased E-selectin expression and monocyte adhesion.

          Conclusions

          This is the first report that 15-oxo-ETE promotes early pathological process of atherosclerosis by accelerating E-selectin expression and monocyte adhesion. 15-oxo-ETE -induced monocyte adhesion is partly attributable to activation of PKC.

          Electronic supplementary material

          The online version of this article (doi:10.1186/s12944-017-0518-2) contains supplementary material, which is available to authorized users.

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          Vascular adhesion molecules in atherosclerosis.

          Elena G. Galkina, Klaus Ley (2007)
          Numerous reports document the role of vascular adhesion molecules in the development and progression of atherosclerosis. Recent novel findings in the field of adhesion molecules require an updated summary of current research. In this review, we highlight the role of vascular adhesion molecules including selectins, vascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule1 (ICAM-1), PECAM-1, JAMs, and connexins in atherosclerosis. The immune system is important in atherosclerosis, and significant efforts are under way to understand the vascular adhesion molecule-dependent mechanisms of immune cell trafficking into healthy and atherosclerosis-prone arterial walls. This review focuses on the role of vascular adhesion molecules in the regulation of immune cell homing during atherosclerosis and discusses future directions that will lead to better understanding of this disease.
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            Biosynthesis, biological effects, and receptors of hydroxyeicosatetraenoic acids (HETEs) and oxoeicosatetraenoic acids (oxo-ETEs) derived from arachidonic acid.

            William Powell, Joshua Rokach (2015)
            Arachidonic acid can be oxygenated by a variety of different enzymes, including lipoxygenases, cyclooxygenases, and cytochrome P450s, and can be converted to a complex mixture of oxygenated products as a result of lipid peroxidation. The initial products in these reactions are hydroperoxyeicosatetraenoic acids (HpETEs) and hydroxyeicosatetraenoic acids (HETEs). Oxoeicosatetraenoic acids (oxo-ETEs) can be formed by the actions of various dehydrogenases on HETEs or by dehydration of HpETEs. Although a large number of different HETEs and oxo-ETEs have been identified, this review will focus principally on 5-oxo-ETE, 5S-HETE, 12S-HETE, and 15S-HETE. Other related arachidonic acid metabolites will also be discussed in less detail. 5-Oxo-ETE is synthesized by oxidation of the 5-lipoxygenase product 5S-HETE by the selective enzyme, 5-hydroxyeicosanoid dehydrogenase. It actions are mediated by the selective OXE receptor, which is highly expressed on eosinophils, suggesting that it may be important in eosinophilic diseases such as asthma. 5-Oxo-ETE also appears to stimulate tumor cell proliferation and may also be involved in cancer. Highly selective and potent OXE receptor antagonists have recently become available and could help to clarify its pathophysiological role. The 12-lipoxygenase product 12S-HETE acts by the GPR31 receptor and promotes tumor cell proliferation and metastasis and could therefore be a promising target in cancer therapy. It may also be involved as a proinflammatory mediator in diabetes. In contrast, 15S-HETE may have a protective effect in cancer. In addition to GPCRs, higher concentration of HETEs and oxo-ETEs can activate peroxisome proliferator-activated receptors (PPARs) and could potentially regulate a variety of processes by this mechanism. This article is part of a Special Issue entitled "Oxygenated metabolism of PUFA: analysis and biological relevance".
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              Endothelial Dysfunction: Clinical Implications in Cardiovascular Disease and Therapeutic Approaches

              Kyoung-Ha Park, Woo Park (2015)
              Atherosclerosis is a chronic progressive vascular disease. It starts early in life, has a long asymptomatic phase, and a progression accelerated by various cardiovascular risk factors. The endothelium is an active inner layer of the blood vessel. It generates many factors that regulate vascular tone, the adhesion of circulating blood cells, smooth muscle proliferation, and inflammation, which are the key mechanisms of atherosclerosis and can contribute to the development of cardiovascular events. There is growing evidence that functional impairment of the endothelium is one of the first recognizable signs of development of atherosclerosis and is present long before the occurrence of atherosclerotic cardiovascular disease. Therefore, understanding the endothelium's central role provides not only insights into pathophysiology, but also a possible clinical opportunity to detect early disease, stratify cardiovascular risk, and assess response to treatments. In the present review, we will discuss the clinical implications of endothelial function as well as the therapeutic issues for endothelial dysfunction in cardiovascular disease as primary and secondary endothelial therapy. Graphical Abstract
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                Author and article information

                Contributors
                Lemin Zheng: +86-10-82805452 , zhengl@bjmu.edu.cn
                Buxing Chen:
                ORCID: http://orcid.org/0000-0001-7473-2739
                010-67096572 , chbux@126.com
                Journal
                Journal ID (nlm-ta): Lipids Health Dis
                Journal ID (iso-abbrev): Lipids Health Dis
                Title: Lipids in Health and Disease
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1476-511X
                Publication date (Electronic): 12 July 2017
                Publication date PMC-release: 12 July 2017
                Publication date Collection: 2017
                Volume: 16
                Electronic Location Identifier: 137
                Affiliations
                [1 ]ISNI 0000 0004 0369 153X, GRID grid.24696.3f, Department of Cardiology, Beijing Tian Tan Hospital, , Capital Medical University, ; Beijing, 100050 China
                [2 ]ISNI 0000 0001 2256 9319, GRID grid.11135.37, The Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, School of Basic Medical Sciences, and Key Laboratory of Molecular Cardiovascular Sciences of Ministry of Education, , Peking University Health Science Center, ; Beijing, 100191 China
                [3 ]Tai Zhou Municipal Hospital, Taizhou, 318000 China
                [4 ]ISNI 0000 0004 1757 9178, GRID grid.415108.9, Department of Cardiovascular Medicine, , Fujian Provincial Hospital, ; Fuzhou, China
                [5 ]ISNI 0000 0004 1758 0478, GRID grid.411176.4, Department of Nephrology, Union Hospital, , Fujian Medical University Union Hospital, ; Fuzhou, China
                Author information
                http://orcid.org/0000-0001-7473-2739
                Article
                Publisher ID: 518
                DOI: 10.1186/s12944-017-0518-2
                PMC ID: 5508789
                PubMed ID: 28701173
                SO-VID: 2f8d39ea-da5d-4afd-91a6-50bbc30084ab
                Copyright © © The Author(s). 2017
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 28 January 2017
                Date accepted : 15 June 2017
                Categories
                Subject: Research
                Custom metadata
                issue-copyright-statement © The Author(s) 2017

                ScienceOpen disciplines: Biochemistry
                Keywords: 15-oxo-ete,monocyte adhesion,e-selectin,atherosclerosis,pkc
                Data availability:
                ScienceOpen disciplines: Biochemistry
                Keywords: 15-oxo-ete, monocyte adhesion, e-selectin, atherosclerosis, pkc

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