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Updated: Jul 14, 2026

Improved Protocol for Chromatin Immunoprecipitation from Mouse Skeletal Muscle

Improved Protocol for Chromatin Immunoprecipitation from Mouse Skeletal Muscle

Published on: November 6, 2017

Programming smooth muscle plasticity with chromatin dynamics.

Oliver G McDonald¹, Gary K Owens

¹Department of Molecular Physiology and Biological Physics, University of Virginia Health Sciences Center, Charlottesville, VA 22903, USA.

Circulation Research

|May 26, 2007

Summary

Smooth muscle cells (SMCs) adapt via phenotypic plasticity, regulated by serum response factor (SRF) and epigenetic histone modifications. This interplay controls SMC differentiation in development and vascular diseases.

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Last Updated: Jul 14, 2026

Improved Protocol for Chromatin Immunoprecipitation from Mouse Skeletal Muscle

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Published on: November 6, 2017

Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers

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CRISPR-Mediated Reorganization of Chromatin Loop Structure

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Published on: September 14, 2018

Area of Science:

Cell Biology
Epigenetics
Vascular Biology

Background:

Smooth muscle cells (SMCs) exhibit significant phenotypic plasticity, crucial for adapting to environmental changes.
Vascular SMCs alter their phenotype during neointimal formation and in atherosclerotic plaques.
Serum response factor (SRF) and cofactors interacting with CArG DNA sequences are key in regulating SMC differentiation.

Purpose of the Study:

To investigate the role of SRF, its cofactors, and histone modifications in SMC differentiation.
To understand how extracellular cues influence SMC phenotype through epigenetic mechanisms.
To explore the dynamic regulation of SMC differentiation at the chromatin level.

Main Methods:

Analysis of SRF-cofactor interactions with CArG box DNA.
Examination of SMC-specific histone modifications in gene promoters.
Investigating the impact of epigenetic modifications on SRF chromatin binding.

Main Results:

SMC differentiation is dynamically regulated by SRF, its cofactors, and CArG box interactions.
SMC-specific histone modifications encode an epigenetic program influencing SRF binding.
Extracellular cues modulate SMC differentiation by altering SRF-chromatin interactions via histone modifications.

Conclusions:

SMC differentiation is a dynamic process controlled by the interplay of SRF, chromatin, and epigenetic modifications.
Understanding these mechanisms offers insights into normal development and vascular disease pathogenesis.
The plasticity of SMCs provides a model for studying dynamic cellular differentiation controlled by chromatin and microenvironments.