Galectin-2 expression is dependent on the rs7291467 polymorphism and acts as an inhibitor of arteriogenesis
| Autor: | José P.S. Henriques, Maurits R. Hollander, Joost O. Fledderus, Karel T. Koch, J.M. Baggen, Jan Baan, Jan J. Piek, Marije M. Vis, A.J.N.M. Bastiaansen, Niels van Royen, Jasper J. Koning, Anton J.G. Horrevoets, Stephan H. Schirmer, Margreet R. de Vries, Anja M. van der Laan, Oscar L. Volger, Tineke C. T. M. van der Pouw Kraan, Paul H.A. Quax, René J. van der Schaaf, Reina E. Mebius |
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| Přispěvatelé: | Molecular cell biology and Immunology, Cardiology, ICaR - Ischemia and repair, Other departments, Amsterdam Cardiovascular Sciences |
| Jazyk: | angličtina |
| Rok vydání: | 2012 |
| Předmět: |
Male
Collateral circulation Lipopolysaccharide Galectin 2 Artery morphogenesis Coronary artery disease Monocytes Mice chemistry.chemical_compound In vivo Galectin-2 Animals Humans Macrophage Medicine RNA Messenger Aged Polymorphism Genetic Genetic polymorphism business.industry Interleukin Cardiovascular Agents Middle Aged Hindlimb Mice Inbred C57BL Coronary Occlusion chemistry Coronary occlusion Immunology Female Interleukin-4 Arteriogenesis Cardiology and Cardiovascular Medicine business |
| Zdroj: | van der Laan, A M, Schirmer, S H, de Vries, M R, Koning, J J, Volger, O L, Fledderus, J O, Bastiaansen, A J N M, Hollander, M R, Baggen, J M, Koch, K T, Baan, J, Henriques, J P, van der Schaaf, R J, Vis, M M, Mebius, R E, van der Pouw Kraan, T, Quax, P H, Piek, J J, Horrevoets, A J G & van Royen, N 2012, ' Galectin-2 expression is dependent on the rs7291467 polymorphism and acts as an inhibitor of arteriogenesis ', European Heart Journal, vol. 33, no. 9, pp. 1076-1084 . https://doi.org/10.1093/eurheartj/ehr220 European Heart Journal, 33(9), 1076-1084. Oxford University Press European Heart Journal, 33(9), 1076-1084 European heart journal, 33(9), 1076-1084. Oxford University Press |
| ISSN: | 0195-668X |
| Popis: | Aims In patients with obstructive coronary artery disease (CAD), the growth of collateral arteries, i.e. arteriogenesis, can preserve myocardial tissue perfusion and function. Monocytes modulate this process, supplying locally the necessary growth factors and degrading enzymes. Knowledge on factors involved in human arteriogenesis is scarce. Thus, the aim of the present study is to identify targets in monocytes that are critical for arteriogenesis in patients with CAD. Methods and results A total of 50 patients with a chronic total coronary occlusion were dichotomized according to their collateral flow index. From each patient, RNA was isolated from unstimulated peripheral blood monocytes, monocytes stimulated by lipopolysaccharide (LPS) or interleukin (IL)-4, and from macrophages. Increased mRNA expression of galectin-2 was found in three out of four monocytic cell types of patients with a low capacity of the collateral circulation ( P = 0.03 for unstimulated monocytes; P = 0.02 for LPS-stimulated monocytes; P = 0.20 for IL-4-stimulated monocytes; P = 0.02 for macrophages). Additionally, galectin-2 mRNA expression was significantly associated with the rs7291467 polymorphism in LGALS2 encoding galectin-2 in all four monocytic cell types. Patient with the rs7291467 CC genotype displayed highest galectin-2 expression, and also tended to have a lower arteriogenic response. To evaluate the effect of galectin-2 on arteriogenesis in vivo , we used a murine hindlimb model. Treatment with galectin-2 markedly impaired the perfusion restoration at Day 7. Conclusion Collectively, these results identify galectin-2 as a novel inhibitor of arteriogenesis. Modulation of galectin-2 may constitute a new therapeutic strategy for the stimulation of arteriogenesis in patients with CAD. |
| Databáze: | OpenAIRE |
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