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Updated: Nov 17, 2025

Quantification of Atherosclerosis in Mice

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

Myeloid Ezh2 Deficiency Limits Atherosclerosis Development.

Annette E Neele¹, Hung-Jen Chen¹, Marion J J Gijbels^1,2

¹Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, Amsterdam Infection and Immunity, Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands.

Frontiers in Immunology

|February 12, 2021

Summary

This summary is machine-generated.

Removing EZH2 in myeloid cells reduces atherosclerosis by impairing neutrophil migration and decreasing inflammatory responses in macrophage foam cells. This epigenetic intervention offers a novel therapeutic strategy for atherosclerosis.

Keywords:

H3K27 PRC2 atherosclerosis epigenetic histone modification macrophage polycomb

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Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice

Published on: February 20, 2019

Area of Science:

Immunology
Epigenetics
Cardiovascular Research

Background:

Macrophages are key immune regulators in atherosclerosis.
Epigenetic modifications, specifically histone methylation, influence macrophage function.
EZH2 catalyzes H3K27 trimethylation, promoting inflammation by suppressing SOCS3.

Purpose of the Study:

To investigate the role of myeloid EZH2 in the development of atherosclerosis.
To determine if targeting myeloid EZH2 could be a therapeutic strategy for atherosclerosis.

Main Methods:

Generated myeloid-specific EZH2-deficient mice (Ezh2del).
Transplanted bone marrow from Ezh2del or wild-type (Ezh2wt) mice into Ldlr-/- mice.
Fed mice a high-fat diet and analyzed atherosclerotic lesion development.

Main Results:

Myeloid EZH2 deficiency significantly reduced atherosclerotic lesion size.
Neutrophil numbers and migratory capacity were decreased in Ezh2del mice.
Ezh2del foam cells exhibited reduced inflammatory responses (nitric oxide, IL-6, IL-12).

Conclusions:

Myeloid EZH2 deficiency impairs neutrophil migration and reduces macrophage inflammatory responses.
Targeting myeloid EZH2 offers a potential therapeutic approach to reduce atherosclerosis.