Resistin-like molecule β is abundantly expressed in foam cells and is involved in atherosclerosis development

Akifumi Kushiyama1, Hideyuki Sakoda, Naohide Oue

  • 1Department of Internal Medicine, The Institute for Adult Diseases, Asahi Life Foundation, Tokyo, Japan.

Abstract

Insights

Resistin-like molecule beta (RELMβ) promotes atherosclerosis by increasing lipid accumulation and inflammation in macrophages. Its absence in knockout mice reduced plaque development, highlighting its role in the disease.

Area of Science:

  • Immunology
  • Cardiovascular Biology
  • Molecular Medicine

Background:

  • Resistin-like molecule beta (RELMβ) is a secretory protein involved in local immune responses.
  • Activated macrophages express RELMβ, suggesting a potential role in inflammatory diseases.

Purpose of the Study:

  • To investigate the role of RELMβ in the development of atherosclerosis.
  • To determine RELMβ's contribution to lipid accumulation and inflammation in macrophages.

Main Methods:

  • Utilized RELMβ knockout and wild-type mice on an apolipoprotein E-deficient background.
  • Analyzed lipid accumulation in atherosclerotic lesions.
  • Assessed macrophage inflammatory response and cytokine secretion in vitro.
  • Investigated the effect of RELMβ stimulation on macrophage gene expression.

Main Results:

  • RELMβ is highly expressed in foam cells within human coronary artery atherosclerotic lesions.
  • RELMβ knockout mice showed reduced lipid accumulation in the aorta.
  • RELMβ deficiency impaired lipopolysaccharide-induced inflammatory pathways and cytokine secretion in macrophages.
  • RELMβ stimulation upregulated inflammatory cytokines and lipid transporters in macrophages.

Conclusions:

  • RELMβ is significantly expressed in atherosclerotic plaques and contributes to disease progression.
  • RELMβ facilitates atherosclerosis by promoting lipid accumulation and inflammation in macrophages.

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