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Related Experiment Video

Updated: Aug 6, 2025

A Method to Study de novo Formation of Chromatin Domains

A Method to Study de novo Formation of Chromatin Domains

Published on: August 23, 2019

Gene-repressing epigenetic reader EED unexpectedly enhances cyclinD1 gene activation.

Mengxue Zhang¹, Jing Li¹, Qingwei Wang¹

¹Department of Surgery, School of Medicine, University of Virginia, Charlottesville, VA 22908, USA.

Molecular Therapy. Nucleic Acids

|March 16, 2023

Summary

Embryonic ectoderm development (EED) unexpectedly activates the CCND1 gene, promoting vascular smooth muscle cell proliferation and neointima formation. Inhibiting EED reduced neointima in vivo, suggesting a new therapeutic target for stenotic diseases.

Keywords:

BRD4 in p57 repression EED in Ccnd1 activation MT: Oligonucleotides: Therapies and Applications cooperativity between EED and BRD4 epigenetic readers neointima smooth muscle cell proliferation

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Area of Science:

Epigenetics
Vascular Biology
Cell Proliferation

Background:

Vascular smooth muscle cell (SMC) proliferation drives neointima formation in stenotic diseases.
Histone marks H3K27me3 (repression) and H3K27ac (activation) regulate gene expression.
Embryonic ectoderm development (EED) is a canonical repressor, reading H3K27me3.

Purpose of the Study:

To investigate the role of EED in vascular smooth muscle cell proliferation and neointima formation.
To elucidate the mechanism by which EED influences gene expression, particularly CCND1.

Main Methods:

Chromatin immunoprecipitation quantitative PCR (ChIP-qPCR) to assess protein-DNA interactions.
Co-immunoprecipitation to study protein-protein interactions.
Pharmacological inhibition of EED and BRD4.
In vivo studies using rat carotid artery injury model and analysis of human neointimal lesions.

Main Results:

EED overexpression increased CCND1 mRNA in SMCs, contradicting its known repressive function.
EED co-immunoprecipitated with BRD4, and they co-occupied CCND1 and P57 gene promoters.
EED inhibition reduced angioplasty-induced neointima formation and cyclinD1 levels in vivo.

Conclusions:

EED unexpectedly activates the pro-proliferative gene CCND1, likely through cooperation with BRD4.
This EED-BRD4 interaction represses anti-proliferative P57, promoting SMC proliferation.
Targeting EED offers a novel epigenetic strategy for treating neointimal hyperplastic disorders.