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Updated: Dec 31, 2025
Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
Published on: February 20, 2019
Selenomethionine supplementation reduces lesion burden, improves vessel function and modulates the inflammatory
Yunjia Zhang1, Siân P Cartland1, Rodney Henriquez1
1Heart Research Institute, 7 Eliza Street, Newtown, Sydney, NSW, 2042, Australia; Sydney Medical School, Edward Ford Building A27, University of Sydney, Sydney, NSW, 2006, Australia.
Insights
Selenomethionine (SeMet) supplementation reduced atherosclerosis in mice by decreasing inflammatory macrophages and improving blood vessel function. This suggests SeMet may be a potential therapeutic strategy for cardiovascular disease.
Area of Science:
- Cardiovascular Research
- Nutritional Immunology
- Vascular Biology
Background:
- Atherosclerosis is a chronic inflammatory vascular disease driven by immune cell infiltration and plaque progression.
- Selenium (Se) and its organic form, selenomethionine (SeMet), are crucial for immune regulation and antioxidant defense.
- Apolipoprotein E deficient (ApoE-/-) mice are a well-established model for studying atherosclerosis.
Purpose of the Study:
- To investigate the therapeutic potential of dietary selenomethionine (SeMet) supplementation in a mouse model of atherosclerosis.
- To evaluate the impact of SeMet on atherosclerotic plaque development, lesion stability, and vascular function.
- To assess SeMet's effect on inflammatory cell behavior and its relevance in a clinical context.
Main Methods:
- Dietary SeMet (2 mg/kg) supplementation was administered to high-fat diet-fed ApoE-/- mice.
- Tissue selenium levels and glutathione peroxidase activity were measured.
- Atherosclerotic plaque burden, lesion phenotype, and aortic function were assessed.
- Inflammatory macrophage accumulation and neutrophil extracellular trap (NET) release were quantified.
- Ex-vivo experiments were conducted on neutrophils from acute coronary syndrome patients.
Main Results:
- SeMet supplementation increased tissue selenium and glutathione peroxidase activity.
- Significant reduction in atherosclerotic plaque formation and improved aortic function were observed.
- SeMet decreased M1 inflammatory macrophage accumulation and NET release in lesions.
- Ex-vivo studies confirmed SeMet's ability to modulate neutrophil inflammatory responses.
Conclusions:
- Dietary SeMet supplementation demonstrates a significant protective effect against atherosclerosis in ApoE-/- mice.
- SeMet improves vascular function and promotes a more stable atherosclerotic plaque phenotype.
- SeMet's anti-inflammatory effects on macrophages and neutrophils suggest its potential as a therapeutic agent for atherosclerosis and related cardiovascular conditions.
Abstract:
Atherosclerosis is a chronic inflammatory disease of the vasculature characterised by the infiltration of activated neutrophils and macrophages at sites of damage within the vessel wall, which contributes to lesion formation and plaque progression. Selenomethionine (SeMet) is an organic form of selenium (Se), an essential trace element that functions in the regulation of the immune response by both bolstering the endogenous thioredoxin and glutathione antioxidant defence systems and by directly scavenging damaging oxidant species. This study evaluated the effect of dietary SeMet supplementation within a high fat diet fed apolipoprotein E deficient (ApoE-/-) mouse model of atherosclerosis. Dietary supplementation with SeMet (2 mg/kg) increased the tissue concentration of Se, and the expression and activity of glutathione peroxidase, compared to non-supplemented controls. Supplementation with SeMet significantly reduced atherosclerotic plaque formation in mouse aortae, resulted in a more stable lesion phenotype and improved vessel function. Concurrent with these results, SeMet supplementation decreased lesion accumulation of M1 inflammatory type macrophages, and decreased the extent of extracellular trap release from phorbol myristate acetate (PMA)-stimulated mouse bone marrow-derived cells. Importantly, these latter results were replicated within ex-vivo experiments on cultured neutrophils isolated from acute coronary syndrome patients, indicating the ability of SeMet to alter the acute inflammatory response within a clinically-relevant setting. Together, these data highlight the potential beneficial effect of SeMet supplementation as a therapeutic strategy for atherosclerosis.
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