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Updated: May 8, 2026

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response
12:50

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response

Published on: September 15, 2017

Proinflammatory stimuli engage Brahma related gene 1 and Brahma in endothelial injury

Fei Fang1, Dewei Chen, Liming Yu

  • 1From the State Key Laboratory of Reproductive Medicine, and Atherosclerosis Research Center, Provincial Key Laboratory of Cardiovascular Disease; and Department of Pathophysiology, Nanjing Medical University, Nanjing, China.

Circulation Research
|August 22, 2013
PubMed

Insights

Brahma related gene 1 (Brg1) and Brahma (Brm) promote leukocyte adhesion in inflammation-driven cardiovascular diseases. Eliminating Brg1/Brm in endothelial cells protects against atherosclerosis, suggesting they are therapeutic targets.

Area of Science:

  • Molecular Biology
  • Cardiovascular Science
  • Epigenetics

Background:

  • Endothelial dysfunction, driven by inflammation, is central to cardiovascular diseases.
  • Leukocyte adhesion to vessel walls, mediated by cell adhesion molecules (CAMs), is a key inflammatory event.
  • The epigenetic regulation of CAMs and their role in disease remain unclear.

Purpose of the Study:

  • To investigate the role of Brahma related gene 1 (Brg1) and Brahma (Brm) in CAM transactivation.
  • To determine the relevance of Brg1 and Brm in the pathogenesis of atherosclerosis.

Main Methods:

  • Assessed Brg1 and Brm expression in endothelial cells and rodent arteries under proinflammatory stimuli.
  • Manipulated Brg1 and Brm levels (overexpression and knockdown) to evaluate effects on CAM transactivation and leukocyte adhesion.
  • Investigated the interaction of Brg1/Brm with nuclear factor κB/p65 at CAM promoters.
  • Analyzed epigenetic modifications and the impact of 17β-estradiol.
  • Utilized an atherosclerosis mouse model (Apoe(-/-)) with endothelial-specific Brg1/Brm deletion.

Main Results:

  • Proinflammatory stimuli increased Brg1 and Brm expression.
  • Brg1/Brm promoted CAM transactivation and leukocyte adhesion; their depletion abrogated these effects.
  • Brg1/Brm interacted with NF-κB/p65, facilitating its recruitment to CAM promoters.
  • Silencing Brg1/Brm disrupted NF-κB/p65 binding kinetics and altered epigenetic changes.
  • 17β-estradiol inhibited Brg1/Brm expression and activity.
  • Endothelial-specific deletion of Brg1/Brm conferred atheroprotection in Apoe(-/-) mice.

Conclusions:

  • Brg1 and Brm integrate inflammatory signals to drive CAM transactivation and endothelial dysfunction.
  • Brg1 and Brm represent potential therapeutic targets for treating inflammation-related cardiovascular diseases.
Abstract

Keywords:
Brg1atherosclerosisendothelial dysfunctionepigeneticsinflammationtranscription

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