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Galectin-2 expression is dependent on the rs7291467 single nucleotide polymorphism and suppresses collateral artery growth

Cardiovascular Pharmacotherapy

Anja van der Laan
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van der Laan, Anja
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List of Authors:

Van der Laan, Schirmer, De Vries, Koning, Volger, Fledderus, Quax, Piek, Horrevoets, Van Royen


In patients with obstructive coronary artery disease (CAD), the remodeling of small arterioles into large collateral arteries is an important natural mechanism to preserve myocardial tissue perfusion. This process is referred to as arteriogenesis, and is critically dependent on mononuclear cells, especially monocytes.

In the present study, we performed whole genome transcriptome analysis of circulating monocytes of patients with a chronic total coronary occlusion. We found increased monocytic mRNA expression of galectin-2 in patients with a low capacity of the collateral circulation. Patients with a genetic substitution (3279C→T) in intron 1 of the galectin-2 gene (rs7291467) displayed decreased mRNA levels of galectin-2 and these patients also had an enhanced arteriogenic response. Galectin-2 was expressed on the surface of monocytes, and in vitro stimulation of monocytes with exogenous galectin-2 changed their cytokine expression profile in a pro-inflammatory direction. In a murine hindlimb model, the administration of galectin-2 markedly impaired collateral artery growth, without apparent systemic effects on the immune system.

Collectively, these results identify galectin-2 as an inhibitor of arteriogenesis, likely due to modulation of the monocytic phenotype. Blockage of galectin-2 may constitute a novel therapeutic strategy for the stimulation of collateral artery growth in patients with CAD.




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The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.