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MS4A6A regulates ox-LDL-induced endothelial dysfunction and monocyte adhesion in atherosclerosis via the

Lu-Chen1, Ke-Wei Yu1, Qi-Zhen Zhuang1

  • 1The Second Clinical College of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510120, China; Department of Laboratory Medicine, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, Guangdong 510120, China.

International Immunopharmacology
|March 16, 2025
PubMed

Insights

Membrane Spanning 4-Domains A6A (MS4A6A) promotes atherosclerosis by increasing endothelial dysfunction and monocyte adhesion via the IKK/NF-κB pathway. Targeting MS4A6A may offer new treatments for cardiovascular diseases.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Molecular Medicine

Background:

  • Atherosclerosis (AS) involves chronic inflammation and endothelial dysfunction, key factors in cardiovascular diseases (CVDs).
  • Membrane Spanning 4-Domains A6A (MS4A6A) is linked to inflammation and immunity, processes relevant to AS pathogenesis.
  • The precise role of MS4A6A in AS development remains largely unelucidated.

Purpose of the Study:

  • To investigate the role and mechanism of MS4A6A in the progression of atherosclerosis.
  • To determine if MS4A6A is a potential therapeutic target for AS.

Main Methods:

  • Bioinformatic analysis of human atherosclerotic plaques.
  • Experimental validation using Western blot, ELISA, immunohistochemistry, and immunofluorescence.
  • In vivo studies with high-cholesterol diet fed ApoE-/- mice.
  • In vitro studies using human umbilical vein endothelial cells (HUVECs) treated with oxidized low-density lipoprotein (ox-LDL).
  • Gene silencing of MS4A6A and pathway analysis involving IκB kinase (IKK)/NF-κB.

Main Results:

  • MS4A6A expression is elevated in human atherosclerotic plaques and correlates with AS severity.
  • MS4A6A is upregulated in endothelial cells of atherosclerotic lesions in mice and in ox-LDL-stimulated HUVECs.
  • Silencing MS4A6A ameliorates endothelial dysfunction, reduces monocyte adhesion, and decreases inflammatory markers and reactive oxygen species (ROS).
  • MS4A6A promotes endothelial dysfunction and monocyte adhesion by activating the IKK/NF-κB signaling pathway.

Conclusions:

  • MS4A6A expression is significantly increased in atherosclerosis and contributes to disease progression.
  • MS4A6A exacerbates endothelial dysfunction and monocyte adhesion through the IKK/NF-κB pathway.
  • MS4A6A represents a potential biomarker and therapeutic target for atherosclerosis and related cardiovascular diseases.

Keywords:
AtherosclerosisEndothelial dysfunctionMS4A6AMonocyte adhesionNF-κB pathway

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