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Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
Published on: September 26, 2018
Regulatory T cells prevent plaque disruption in apolipoprotein E-knockout mice
Xiao Meng1, Wenjun Li, Jianmin Yang
1The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Qilu Hospital, Shandong University, Jinan, China.
International Journal of Cardiology
|April 10, 2013
Summary
Regulatory T cells (Tregs) stabilize atherosclerotic plaques by reducing inflammation and matrix metalloproteinases, and increasing collagen. This dose-dependent treatment offers a novel therapeutic approach for vulnerable plaques.
Area of Science:
- Immunology
- Cardiovascular Research
- Atherosclerosis
Background:
- CD4(+)CD25(+) regulatory T cells (Tregs) are implicated in atherogenesis.
- Atherosclerotic plaques are characterized by inflammation and matrix degradation.
Purpose of the Study:
- To investigate the dose-dependent effects of Tregs on atherosclerotic plaque stability.
- To elucidate the mechanisms by which Tregs stabilize plaques.
Main Methods:
- A vulnerable carotid plaque model was established in apolipoprotein E-knockout (ApoE-/-) mice.
- Mice received varying doses of Tregs, phosphate-buffered saline (PBS), or placebo.
- Histopathological analysis assessed plaque disruption, composition, and molecular markers.
Main Results:
- Tregs treatment dose-dependently reduced plaque disruption and vulnerability.
- Tregs decreased macrophages and lipids while increasing smooth muscle cells and collagen.
- Tregs inhibited inflammatory cytokines, MMP-2, and MMP-9, and enhanced P4Hα1 expression.
Conclusions:
- Adoptive transfer of Tregs dose-dependently promotes plaque stability in ApoE-/- mice.
- Mechanisms include reduced inflammation and MMPs, and enhanced P4Hα1.
- Tregs represent a promising novel therapy for vulnerable atherosclerotic plaques.
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