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Effect of hyperlipidemia on Foxp3 expression in apolipoprotein E-knockout mice
Zhixiao Wang1, Shan Mao, Zhongqun Zhan
1Department of Cardiology, Taihe Hospital, Hubei University of Medicine, Shiyan, China.
Journal of Cardiovascular Medicine (Hagerstown, Md.)
|April 5, 2014
Summary
High-fat diets impair the expression and function of the transcription factor forkhead box P3 (Foxp3) in regulatory T cells. This may contribute to atherosclerosis development in hyperlipidemia.
Area of Science:
- Immunology
- Cardiovascular Science
- Molecular Biology
Background:
- Forkhead box P3 (Foxp3) is crucial for regulatory T cell development and function.
- Regulatory T cells play a key role in maintaining immune homeostasis.
Purpose of the Study:
- To investigate the impact of hyperlipidemia on Foxp3 expression in mice.
- To understand the molecular mechanisms linking hyperlipidemia to immune dysfunction.
Main Methods:
- Apolipoprotein E (ApoE) mice were fed a high-fat diet or control diet.
- Assessed plasma lipid levels, regulatory T cell populations (Foxp3+CD4+CD25+), and atherosclerotic lesion size.
- Quantified Foxp3 gene and protein expression in various tissues.
Main Results:
- High-fat diet significantly elevated plasma lipid levels.
- Reduced numbers and function of Foxp3+ regulatory T cells were observed in hyperlipidemic mice.
- Decreased Foxp3 protein and gene expression in immune organs of the high-fat diet group.
Conclusions:
- Hyperlipidemia suppresses Foxp3 expression and regulatory T cell function.
- Inhibition of Foxp3 may be a mechanism by which hyperlipidemia exacerbates atherosclerosis.
- Findings highlight a link between metabolic dysfunction and immune regulation in cardiovascular disease.
