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Updated: May 29, 2026

Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
Mononuclear cell therapy attenuates atherosclerosis in apoE KO mice
Marcella L Porto1, Leandro C F Lima, Thiago M C Pereira
1Laboratory of Transgenes and Cardiovascular Control, Dept Physiological Sciences, Health Sciences Center, Federal University of Espirito Santo, Vitoria, ES, Brazil.
Mononuclear cell (MNC) therapy significantly reduced atherosclerosis progression in apolipoprotein E knockout mice. This cell therapy approach involves the homing of endothelial progenitor cells (EPCs), decreasing oxidative stress and increasing eNOS expression.
Area of Science:
- Cardiovascular Research
- Regenerative Medicine
- Immunology
Background:
- Atherosclerosis is a chronic inflammatory disease characterized by lipid deposition and plaque formation in arteries.
- Cell therapy is emerging as a potential treatment strategy for cardiovascular diseases.
- The apolipoprotein E knockout (apoE KO) mouse model is widely used to study atherosclerosis.
Purpose of the Study:
- To evaluate the therapeutic effects of mononuclear cell (MNC) therapy on the development of atherosclerotic lesions in apoE KO mice.
- To investigate the impact of MNC therapy on vascular lipid deposition, remodeling, oxidative stress, and endothelial nitric oxide synthase (eNOS) expression.
Main Methods:
- ApoE KO mice were treated with spleen MNCs for 8 weeks.
- Vascular lipid deposition and remodeling were assessed via histological analysis and morphometry.
- Oxidative stress markers and eNOS expression were quantified.
- Immunohistochemistry was used to detect the homing of endothelial progenitor cells (EPCs).
Main Results:
- MNC therapy significantly reduced lipid deposition in the aortas of apoE KO mice.
- MNC treatment prevented outward vascular remodeling compared to untreated controls.
- Treated mice exhibited reduced superoxide anion production and increased eNOS expression.
- Evidence of EPC homing in the aortas of MNC-treated mice was observed.
Conclusions:
- MNC therapy effectively attenuates atherosclerosis progression in the apoE KO mouse model.
- The therapeutic mechanism involves EPC homing, reduced oxidative stress, and enhanced eNOS expression.
- These findings support MNC therapy as a promising strategy for treating atherosclerosis.
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