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Culture of Macrophage Colony-stimulating Factor Differentiated Human Monocyte-derived Macrophages
Published on: June 30, 2016
The Dynamics of Circulating Monocyte Subsets and Intra-Plaque Proliferating Macrophages during the Development of
Jun-Xiang Liu1, Xiao Li2, Wen-Jie Ji1
1Tianjin Key Laboratory of Cardiovascular Remodeling and Target Organ Injury, Pingjin Hospital Heart Center, Logistics University of PAPF.
Abstract:
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 Ly6Chi 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 Ly6Chi 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 Ly6Chi 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.
Insights
Atherosclerosis development in ApoE-/- mice shows elevated Ly6Chi monocytes and proliferative macrophages, with levels plateauing over time despite diet changes. Macrophage density remained stable throughout the study.
Area of Science:
- Cardiovascular Biology
- Immunology
- Atherosclerosis Research
Background:
- Atherosclerosis is a chronic inflammatory disease characterized by plaque buildup in arteries.
- Monocytes and macrophages play critical roles in the development and progression of atherosclerotic lesions.
- Understanding the dynamic changes of these immune cells is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the dynamic changes in monocyte subsets and macrophage populations during atherosclerosis development in ApoE-/- mice.
- To correlate these cellular changes with lipid profiles and lesion progression.
- To provide insights for novel therapeutic strategies targeting mononuclear phagocytes.
Main Methods:
- Atherosclerosis was induced in 84 ApoE-/- mice fed either a western or chow diet.
- Mice were euthanized at various time points (2-12 weeks) for analysis.
- Flow cytometry, confocal microscopy, and Oil Red O staining were used to assess monocyte subsets, macrophage density, and lesion area.
Main Results:
- Ly6C(hi) circulating monocytes and proliferative macrophages in ApoE-/- mice peaked at 8 and 6 weeks, respectively, then plateaued.
- Total plasma cholesterol, triglyceride levels, and aortic sinus lesion area were elevated in both diet groups, with higher levels in the western diet group.
- Macrophage density within plaques did not significantly change with age in either diet group.
Conclusions:
- The study provides a dynamic overview of Ly6C(hi) monocyte and macrophage changes during atherosclerosis progression in ApoE-/- mice.
- Mononuclear phagocyte dynamics, particularly Ly6C(hi) monocytes and proliferative macrophages, exhibit distinct temporal patterns.
- These findings are relevant for designing future therapeutic interventions targeting specific immune cell populations in atherosclerosis.
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