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Galectin-2 expression is dependent on the rs7291467 polymorphism and acts as an inhibitor of arteriogenesis

Anja M van der Laan1, Stephan H Schirmer, Margreet R de Vries

  • 1Department of Cardiology, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands.

European Heart Journal
|August 12, 2011
PubMed

Insights

Galectin-2 inhibits arteriogenesis, the growth of collateral arteries in coronary artery disease (CAD) patients. Targeting galectin-2 may offer a new therapeutic strategy to improve blood flow in CAD.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Molecular Medicine

Background:

  • Arteriogenesis, the growth of collateral arteries, is crucial for preserving heart function in obstructive coronary artery disease (CAD).
  • Monocytes play a key role in arteriogenesis by supplying growth factors and enzymes.
  • Understanding factors influencing human arteriogenesis is limited.

Purpose of the Study:

  • To identify monocyte-specific targets critical for arteriogenesis in patients with CAD.
  • To investigate the role of galectin-2 in the process of arteriogenesis.

Main Methods:

  • Analysis of monocytes and macrophages from 50 CAD patients with varying collateral flow.
  • Measurement of galectin-2 mRNA expression in different monocyte stimulation states.
  • Evaluation of galectin-2's effect on arteriogenesis using a murine hindlimb model.

Main Results:

  • Elevated galectin-2 mRNA expression was observed in monocytes and macrophages of patients with poor collateral circulation.
  • Galectin-2 expression correlated with a specific polymorphism (rs7291467) in the LGALS2 gene.
  • In vivo studies demonstrated that galectin-2 treatment impaired perfusion restoration.

Conclusions:

  • Galectin-2 acts as a novel inhibitor of arteriogenesis.
  • Modulating galectin-2 presents a potential therapeutic avenue for stimulating arteriogenesis in CAD patients.
Abstract

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