2017

DOI: 10.1536/ihj.17-552

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Omega-3 Polyunsaturated Fatty Acid and Coronary Atherosclerotic Plaques

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Hiroyuki Morita

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“…[1][2][3][4] Recent basic studies have shown that monocytes/macrophages are major players in atherosclerosis. [5][6][7] Specifically, hyperlipidemiainduced proinflammatory Ly6C hi monocytosis, via a CCR2-dependent mechanism, 8,9) contributes to monocyte sub-endothelial infiltration and plaque destabilization, and ultimately ischemic cardiovascular events. 10) Additionally, the human proinflammatory monocyte counterpart, i.e., the CD14 ++ CD16 + subset, whose level is elevated during hyperlipidemia and after cerebral and myocardial ischemia, is associated with the occurrence of acute coronary syndrome and poor prognosis after cerebral and myocardial ischemia.…”

mentioning

confidence: 99%

The Dynamics of Circulating Monocyte Subsets and Intra-Plaque Proliferating Macrophages during the Development of Atherosclerosis in <i>ApoE</i><sup>−/−</sup> Mice

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et al. 2019

Int. Heart J.

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To detect the development of monocytes and proliferative macrophages in atherosclerosis of ApoE −/− mice, we randomly assigned 84 ApoE −/− mice fed western diet or chow diet. On weeks 2, 4, 6, 8, 10, and 12 after fed high-fat diet or normal chow diet, animals were euthanized (n = 7 for each group at each time point). Flow cytometry methods were used to analyze the proportions of circulation monocyte subsets. The macrophage and proliferative macrophage accumulation within atherosclerotic plaques was estimated by confocal florescence microscopy. Plasma levels of total cholesterol and triglyceride were measured by ELISA kit. The plaques of aortic sinus were stained with Oil Red O. The percent of Ly6C hi circulation monocyte, the density of proliferation macrophage, the total plasma cholesterol and triglyceride levels, the lesion area of ApoE −/− mice were consistently elevated in chow diet throughout the trial. The total plasma cholesterol and triglyceride levels, the lesion area were elevated in western diet group with age, and they were always higher than the chow diet group. The Ly6C hi monocytes and proliferative macrophages reached a plateau at 8 weeks and 6 weeks; despite continued high-triglyceride high-cholesterol diet the percent did not significantly change. Interestingly, the density of macrophage did not change significantly over age in western and chow diet groups. Our results provide a dynamic view of Ly6C hi monocyte subset, the density of macrophage and proliferation macrophage change during the development and progression of atherosclerosis, which is relevant for designing new treatment strategies targeting mononuclear phagocytes in this model.

“…[1][2][3][4] Recent basic studies have shown that monocytes/macrophages are major players in atherosclerosis. [5][6][7] Specifically, hyperlipidemiainduced proinflammatory Ly6C hi monocytosis, via a CCR2-dependent mechanism, 8,9) contributes to monocyte sub-endothelial infiltration and plaque destabilization, and ultimately ischemic cardiovascular events. 10) Additionally, the human proinflammatory monocyte counterpart, i.e., the CD14 ++ CD16 + subset, whose level is elevated during hyperlipidemia and after cerebral and myocardial ischemia, is associated with the occurrence of acute coronary syndrome and poor prognosis after cerebral and myocardial ischemia.…”

mentioning

confidence: 99%

The Dynamics of Circulating Monocyte Subsets and Intra-Plaque Proliferating Macrophages during the Development of Atherosclerosis in <i>ApoE</i><sup>−/−</sup> Mice

¹

,

²

,

³

et al. 2019

Int. Heart J.

View full text Add to dashboard Cite

To detect the development of monocytes and proliferative macrophages in atherosclerosis of ApoE −/− mice, we randomly assigned 84 ApoE −/− mice fed western diet or chow diet. On weeks 2, 4, 6, 8, 10, and 12 after fed high-fat diet or normal chow diet, animals were euthanized (n = 7 for each group at each time point). Flow cytometry methods were used to analyze the proportions of circulation monocyte subsets. The macrophage and proliferative macrophage accumulation within atherosclerotic plaques was estimated by confocal florescence microscopy. Plasma levels of total cholesterol and triglyceride were measured by ELISA kit. The plaques of aortic sinus were stained with Oil Red O. The percent of Ly6C hi circulation monocyte, the density of proliferation macrophage, the total plasma cholesterol and triglyceride levels, the lesion area of ApoE −/− mice were consistently elevated in chow diet throughout the trial. The total plasma cholesterol and triglyceride levels, the lesion area were elevated in western diet group with age, and they were always higher than the chow diet group. The Ly6C hi monocytes and proliferative macrophages reached a plateau at 8 weeks and 6 weeks; despite continued high-triglyceride high-cholesterol diet the percent did not significantly change. Interestingly, the density of macrophage did not change significantly over age in western and chow diet groups. Our results provide a dynamic view of Ly6C hi monocyte subset, the density of macrophage and proliferation macrophage change during the development and progression of atherosclerosis, which is relevant for designing new treatment strategies targeting mononuclear phagocytes in this model.

“…Note that atherosclerotic lesions are characterized by persistent inflammatory responses, which involve macrophages and smooth muscle cells (SMCs) [7][8][9] as well as membrane-anchored forms of heparin-binding epidermal growth factor-like growth factor (HB-EGF), a diphtheria toxin receptor. After binding, this receptor is internalized 10) and excessively expressed in macrophages and SMCs within atherosclerotic plaques.…”

mentioning

confidence: 99%

Anti-HB-EGF Antibody-Mediated Delivery of siRNA to Atherosclerotic Lesions in Mice

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et al. 2018

Int. Heart J.

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For atherosclerotic cardiovascular diseases (ACD), gene therapy may be a potential therapeutic strategy; however, lack of effective and safe methods for gene delivery to atherosclerotic plaques have limited its potential therapeutic applications. To overcome this limitation, we developed a novel antibody-based gene delivery system (anti-HB-EGF/NA vector) by chemically crosslinking antibodies against human heparin-binding epidermal growth factor-like growth factor (HB-EGF). It has been shown to be excessively expressed in human atherosclerotic plaques and NeutrAvidin (NA) for conjugating biotinylated siRNA. Immunofluorescence staining and quantitative flow cytometry analysis using human HB-EGF-expressing cells showed both antibody-mediated selective cellular targeting and efficient intracellular delivery of conjugated biotin-fluorescence. Moreover, we demonstrated antibody-mediated significant and selective gene knockdown via conjugation with anti-HB-EGF/ NA vector and biotinylated siRNA (anti-HB-EGF/NA/b-siRNA) in vitro. Furthermore, using high fat-fed human HB-EGF knock-in and apolipoprotein E-knockout (Hbegf hz/hz; Apoe-/-) mice, we demonstrated that the anti-HB-EGF/NA vector, conjugating biotin-fluorescence, increasingly accumulated within the atherosclerotic plaques of the ascending aorta in which human HB-EGF expression levels were highly elevated. Moreover, in response to a single intravenous injection of anti-HB-EGF/NA/b-siRNA in a dose-dependent manner, qPCR analysis of laser-dissected atherosclerotic plaques of the ascending aorta showed significant knockdown of the reporter gene expression. These results suggest that the anti-HB-EGF antibody-mediated siRNA delivery could be a promising delivery system for gene therapy of ACD.

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