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      Eugenol Inhibits Ox-LDL-Induced Proliferation and Migration of Human Vascular Smooth Muscle Cells by Inhibiting the Ang II/MFG-E8/MCP-1 Signaling Cascade

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          Abstract

          Objective

          In this study, we investigated the effect and mechanism of action of eugenol on oxidized low-density lipoprotein (ox-LDL)-induced abnormal proliferation and migration of human vascular smooth muscle cells (HVSMCs).

          Methods

          HVSMCs were treated with 100 ug/mL ox-LDL for 24 hours to establish a cell model. After 1-hour pretreatment, eugenol at concentrations of 5, 25, and 50 uM was added. Cell viability was assessed using an MTT assay, PCNA expression was detected using Western blot, cell cycle distribution was analyzed using flow cytometry, and cell migration ability was evaluated using wound healing and Transwell migration assays. To investigate the mechanisms, Ang II receptors were inhibited by 1000 nM valsartan, MFG-E8 was knocked down by shRNA, MCP-1 was inhibited by siRNA, and MFG-E8 was overexpressed using plasmids.

          Results

          The findings from this study elucidated the stimulatory impact of ox-LDL on the proliferation and functionality of HVSMCs. Different concentrations of eugenol effectively mitigated the enhanced activity of HVSMCs induced by ox-LDL, with 50 uM eugenol exhibiting the most pronounced inhibitory effect. Flow cytometry and Western blot results showed ox-LDL reduced G1 phase cells and increased PCNA expression, while 50 uM eugenol inhibited ox-LDL-induced HVSMC proliferation. In wound healing and Transwell migration experiments, the ox-LDL group showed larger cell scratch filling and migration than the control group, both of which were inhibited by 50 uM eugenol. Inhibiting the Ang II/MFG-E8/MCP-1 signaling cascade mimicked eugenol’s effects, while MFG-E8 overexpression reversed eugenol’s inhibitory effect.

          Conclusion

          Eugenol can inhibit the proliferation and migration of ox-LDL-induced HVSMCs by inhibiting Ang II/MFG-E8/MCP-1 signaling cascade, making it a potential therapeutic drug for atherosclerosis.

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          Most cited references32

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          Vascular smooth muscle cells in atherosclerosis

          Gemma Basatemur, Helle Jørgensen, Murray Clarke … (2019)
          Vascular smooth muscle cells (VSMCs) are a major cell type present at all stages of an atherosclerotic plaque. According to the 'response to injury' and 'vulnerable plaque' hypotheses, contractile VSMCs recruited from the media undergo phenotypic conversion to proliferative synthetic cells that generate extracellular matrix to form the fibrous cap and hence stabilize plaques. However, lineage-tracing studies have highlighted flaws in the interpretation of former studies, revealing that these studies had underestimated both the content and functions of VSMCs in plaques and have thus challenged our view on the role of VSMCs in atherosclerosis. VSMCs are more plastic than previously recognized and can adopt alternative phenotypes, including phenotypes resembling foam cells, macrophages, mesenchymal stem cells and osteochondrogenic cells, which could contribute both positively and negatively to disease progression. In this Review, we present the evidence for VSMC plasticity and summarize the roles of VSMCs and VSMC-derived cells in atherosclerotic plaque development and progression. Correct attribution and spatiotemporal resolution of clinically beneficial and detrimental processes will underpin the success of any therapeutic intervention aimed at VSMCs and their derivatives.
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            Inflammation in atherosclerosis.

            Peter Libby (2012)
            Experimental work has elucidated molecular and cellular pathways of inflammation that promote atherosclerosis. Unraveling the roles of cytokines as inflammatory messengers provided a mechanism whereby risk factors for atherosclerosis can alter arterial biology, and produce a systemic milieu that favors atherothrombotic events. The discovery of the immune basis of allograft arteriosclerosis demonstrated that inflammation per se can drive arterial hyperplasia, even in the absence of traditional risk factors. Inflammation regulates aspects of plaque biology that trigger the thrombotic complications of atherosclerosis. Translation of these discoveries to humans has enabled both novel mechanistic insights and practical clinical advances.
            Article 0 comments Cited 334 times – based on 0 reviews     Review now
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              Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology

              Steven J. Forrester, George Booz, Curt Sigmund … (2018)
              The renin-angiotensin-aldosterone system plays crucial roles in cardiovascular physiology and pathophysiology. However, many of the signaling mechanisms have been unclear. The angiotensin II (ANG II) type 1 receptor (AT 1 R) is believed to mediate most functions of ANG II in the system. AT 1 R utilizes various signal transduction cascades causing hypertension, cardiovascular remodeling, and end organ damage. Moreover, functional cross-talk between AT 1 R signaling pathways and other signaling pathways have been recognized. Accumulating evidence reveals the complexity of ANG II signal transduction in pathophysiology of the vasculature, heart, kidney, and brain, as well as several pathophysiological features, including inflammation, metabolic dysfunction, and aging. In this review, we provide a comprehensive update of the ANG II receptor signaling events and their functional significances for potential translation into therapeutic strategies. AT 1 R remains central to the system in mediating physiological and pathophysiological functions of ANG II, and participation of specific signaling pathways becomes much clearer. There are still certain limitations and many controversies, and several noteworthy new concepts require further support. However, it is expected that rigorous translational research of the ANG II signaling pathways including those in large animals and humans will contribute to establishing effective new therapies against various diseases.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Inflamm Res
                Journal ID (iso-abbrev): J Inflamm Res
                Journal ID (publisher-id): jir
                Title: Journal of Inflammation Research
                Publisher: Dove
                ISSN (Electronic): 1178-7031
                Publication date (Electronic): 02 February 2024
                Publication date Collection: 2024
                Volume: 17
                Pages: 641-653
                Affiliations
                [1 ]Department of Cardiology, The First Hospital of Jilin University , Changchun, 13000, People’s Republic of China
                [2 ]Department of Experimental Pharmacology and Toxicology, College of Pharmacy, Jilin University , Changchun, 130000, People’s Republic of China
                Author notes
                Correspondence: Yu-Shi Wang, Department of Cardiology, The First Hospital of Jilin University , Changchun, 13000, People’s Republic of China, Tel +86 18643199605, Email yushi@jlu.edu.cn
                [*]

                These authors contributed equally to this work

                Article
                Publisher ID: 446960
                DOI: 10.2147/JIR.S446960
                PMC ID: 10847669
                PubMed ID: 38328560
                SO-VID: 6cf1cea7-cc07-4081-bcae-cca0e52406ef
                Copyright © © 2024 He et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 27 October 2023
                Date accepted : 20 January 2024
                Page count
                Figures: 5, References: 32, Pages: 13
                Funding
                Funded by: Health Talents Special Fund;
                Jilin Province Medical and Health Talents Special Fund, Grant/Award Number: JLSWSRCZX2023-75.
                Categories
                Subject: Original Research

                ScienceOpen disciplines: Immunology
                Keywords: ang ii,eugenol,hvsmcs,mfg-e8,mcp-1,ox-ldl
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: ang ii, eugenol, hvsmcs, mfg-e8, mcp-1, ox-ldl

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