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Updated: Feb 16, 2026
Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus
Published on: December 7, 2013
Annexin A5 reduces early plaque formation in ApoE -/- mice
Robert Stöhr1,2, Leon Schurgers2, Rick van Gorp2
1Medizinische Klinik I, RWTH Aachen University, Aachen, Germany.
Abstract:
Annexin A5 (AnxA5) exerts anti-inflammatory, anticoagulant and anti-apoptotic effects through its binding to cell surface expressed phosphatidylserine. We previously showed that AnxA5 can stabilize advanced atherosclerotic plaques by reducing macrophage infiltration. We now investigated the effects of AnxA5 administration on the onset of atherosclerosis development. Eight-week-old ApoE-/-mice were fed a western diet while being administered AnxA5 or control (M1234) for a total of 6 weeks. AnxA5 administration reduced plaque size in the aortic root as well as the aortic arch by 36% and 55% respectively. As determined by immunohistochemistry, administration of AnxA5 further stabilized plaque by reducing macrophage content and increasing smooth muscle cell content. Furthermore, the pre-treatment of HUVEC's with AnxA5 reduced monocyte adhesion under flow-conditions. Finally, AnxA5 administration results in a trend to reduced cell death more pronounced in the aortic arch than the aortic root. In conclusion, treatment with AnxA5 before the onset of atherosclerosis reduces plaque formation in a murine model of atherosclerosis in part by reducing apoptotic rates further to its beneficial effect on macrophage infiltration and activation.
Insights
Annexin A5 (AnxA5) treatment before atherosclerosis onset reduced plaque formation and size in mice. This protein also decreased macrophage infiltration and cell death, stabilizing plaques.
Area of Science:
- Cardiovascular Biology
- Immunology
- Pharmacology
Background:
- Annexin A5 (AnxA5) is known for its anti-inflammatory, anticoagulant, and anti-apoptotic properties.
- AnxA5 binds to phosphatidylserine on cell surfaces, influencing cellular processes.
- Previous studies demonstrated AnxA5's ability to stabilize advanced atherosclerotic plaques by reducing macrophage infiltration.
Purpose of the Study:
- To investigate the effects of AnxA5 administration on the early development of atherosclerosis.
- To determine if prophylactic AnxA5 treatment can prevent or reduce atherosclerotic plaque formation.
Main Methods:
- Atherosclerosis was induced in eight-week-old ApoE-/- mice using a western diet for 6 weeks.
- Mice received either AnxA5 or a control (M1234) treatment throughout the study period.
- Plaque size, macrophage content, smooth muscle cell content, monocyte adhesion, and cell death rates were analyzed.
Main Results:
- AnxA5 administration significantly reduced plaque size in the aortic root (36%) and aortic arch (55%).
- Immunohistochemistry revealed reduced macrophage content and increased smooth muscle cell content in AnxA5-treated mice, indicating plaque stabilization.
- Pre-treatment with AnxA5 decreased monocyte adhesion to HUVECs under flow conditions.
- A trend towards reduced cell death was observed with AnxA5 treatment, particularly in the aortic arch.
Conclusions:
- Prophylactic treatment with Annexin A5 effectively reduces atherosclerotic plaque formation in a murine model.
- AnxA5's beneficial effects are partly mediated by reducing apoptotic rates and improving macrophage infiltration and activation.
- AnxA5 demonstrates potential as a therapeutic agent for preventing atherosclerosis development.
