Abstract

Heart failure after myocardial infarction (MI) depends on infarct size and adverse left ventricular (LV) remodelling, both influenced by the inflammatory response. Leukocyte-associated immunoglobulin-like receptor 1 (LAIR-1) is an inhibitory receptor of ITAM-dependent cell activation, present on almost all immune cells. We investigated regulation of LAIR-1 leukocyte expression after MI in patients and hypothesized that its absence in a mouse model of MI would increase infarct size and adverse remodelling. In patients, LAIR-1 expression was increased 3 days compared to 6 weeks after MI on circulating monocytes (24.8 ± 5.3 vs. 21.2 ± 5.1 MFI, p = 0.008) and neutrophils (12.9 ± 4.7 vs. 10.6 ± 3.1 MFI, p = 0.046). In WT and LAIR-1−/− mice, infarct size after ischemia-reperfusion injury was comparable (37.0 ± 14.5 in WT vs. 39.4 ± 12.2% of the area at risk in LAIR-1−/−, p = 0.63). Remodelling after permanent left coronary artery ligation did not differ between WT and LAIR-1−/− mice (end-diastolic volume 133.3 ± 19.3 vs. 132.1 ± 27.9 μL, p = 0.91 and end-systolic volume 112.1 ± 22.2 vs. 106.9 ± 33.5 μL, p = 0.68). Similarly, no differences were observed in inflammatory cell influx or fibrosis. In conclusion, LAIR-1 expression on monocytes and neutrophils is increased in the acute phase after MI in patients, but the absence of LAIR-1 in mice does not influence infarct size, inflammation, fibrosis or adverse cardiac remodelling.

Details

Title
Leukocyte-Associated Immunoglobulin-like Receptor-1 is regulated in human myocardial infarction but its absence does not affect infarct size in mice
Author
Guilielmus H J M Ellenbroek 1 ; de Haan, Judith J 1 ; van Klarenbosch, Bas R 2 ; Brans, Maike A D 1 ; Sander M van de Weg 1 ; Smeets, Mirjam B 1 ; de Jong, Sanne 3 ; Arslan, Fatih 4 ; Timmers, Leo 2 ; Goumans, Marie-José T H 5 ; Hoefer, Imo E 6 ; Doevendans, Pieter A 7 ; Pasterkamp, Gerard 6 ; Linde Meyaard 8 ; Saskia C A de Jager 9 

 Laboratory of Experimental Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands 
 Department of Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands 
 Department of Medical Physiology, University Medical Center Utrecht, Utrecht, The Netherlands 
 Laboratory of Experimental Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands; Department of Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands 
 Department of Molecular Cell Biology, Leiden University Medical Center, Leiden, The Netherlands 
 Laboratory of Experimental Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands; Department of Clinical Chemistry and Haematology, University Medical Center Utrecht, Utrecht, The Netherlands 
 Department of Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands; Netherlands Heart Institute, Utrecht, The Netherlands 
 Laboratory of Translational Immunology, Department of Immunology, University Medical Center Utrecht, Utrecht, The Netherlands 
 Laboratory of Experimental Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands; Laboratory of Translational Immunology, Department of Immunology, University Medical Center Utrecht, Utrecht, The Netherlands 
First page
1
Publication year
2017
Publication date
Dec 2017
Publisher
Nature Publishing Group
e-ISSN
20452322
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
1983428970
Copyright
© 2017. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.