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A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
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Un-JAMming atherosclerotic arteries: JAM-L as a target to attenuate plaque development

B Sumayyah H Sokeechand1, Bernardo L Trigatti2

  • 1Department of Biochemistry and Biomedical Sciences and Thrombosis and Atherosclerosis Research Institute, McMaster University, Hamilton, Ontario, Canada.

Clinical Science (London, England : 1979)
|July 24, 2019
PubMed

Insights

Junction adhesion molecule-like (JAML) protein drives inflammation in atherosclerosis. Silencing JAML reduces plaque progression and inflammatory cytokine production, offering a potential therapeutic target for heart attack and stroke prevention.

Area of Science:

  • Cardiovascular biology
  • Immunology
  • Molecular medicine

Background:

  • Atherosclerosis is a chronic inflammatory disease linked to heart attack and stroke.
  • Leukocyte infiltration, macrophage differentiation, and oxidized LDL uptake drive plaque development.
  • Macrophage activation and cytokine production sustain inflammation and plaque growth.

Purpose of the Study:

  • To investigate the role of junction adhesion molecule-like (JAML) protein in atherosclerotic plaque inflammation.
  • To identify novel pathways for therapeutic intervention in atherosclerosis.

Main Methods:

  • Analysis of JAML expression in human and mouse atherosclerotic plaques.
  • Assessment of JAML's role in atherosclerotic plaque progression using mouse models.
  • Investigation of JAML's effect on macrophage inflammatory cytokine production induced by oxidized low-density lipoprotein (OxLDL).

Main Results:

  • JAML is expressed in macrophages and other cells within atherosclerotic plaques.
  • Silencing JAML expression significantly reduces atherosclerotic plaque progression in mouse models.
  • JAML is essential for OxLDL-induced inflammatory cytokine production by macrophages.

Conclusions:

  • JAML plays a critical role in driving atherosclerotic plaque inflammation.
  • Targeting JAML may offer a novel therapeutic strategy to reduce plaque inflammation and progression.
  • JAML represents a potential therapeutic target for managing atherosclerosis and its complications.

Keywords:
AtherosclerosisInflammationJam-LMacrophages

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