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Involvement of leukotactin-1, a novel CC chemokine, in human atherosclerosis

Rina Yu1, Chu-Sook Kim, Teruo Kawada

  • 1Department of Food Science and Nutrition, University of Ulsan, Ulsan 680-749, South Korea. rinayu@ulsan.ac.kr

Atherosclerosis
|May 12, 2004
PubMed

Insights

Leukotactin-1 (Lkn-1) is elevated in atherosclerosis, promoting leukocyte recruitment and ICAM-1 release. This suggests Lkn-1 is a key factor in the development of this chronic inflammatory disease.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Molecular Medicine

Background:

  • Atherosclerosis is a chronic inflammatory condition characterized by leukocyte accumulation in arteries.
  • Leukotactin-1 (Lkn-1), a CC chemokine, attracts leukocytes and is linked to inflammatory diseases.

Purpose of the Study:

  • To investigate the association between Leukotactin-1 (Lkn-1) and human atherosclerosis.
  • To determine the role of Lkn-1 in the development of atherosclerotic lesions.

Main Methods:

  • Quantitative analysis of Lkn-1 mRNA and receptor expression in atherosclerotic lesions and foam cells using RT-PCR.
  • Measurement of plasma Lkn-1, MCP-1, and ICAM-1 levels via ELISA in patients and controls.
  • In vitro studies on Lkn-1 release from macrophages under oxidative stress.

Main Results:

  • Lkn-1 mRNA and circulating levels were significantly higher in atherosclerosis patients compared to normal subjects.
  • Oxidative stress and proatherogenic mediators increased Lkn-1 release from macrophages and foam cells.
  • Lkn-1 stimulated endothelial cells to release ICAM-1, a molecule involved in atherogenesis.

Conclusions:

  • Lkn-1 expression is upregulated in human atherosclerosis at both mRNA and plasma levels.
  • Lkn-1 release is enhanced by conditions mimicking the atherosclerotic environment.
  • Lkn-1 contributes to atherogenesis by promoting leukocyte adhesion via ICAM-1 induction.

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