| First Author | Ellenbroek GHJM | Year | 2017 |
| Journal | Sci Rep | Volume | 7 |
| Issue | 1 | Pages | 18039 |
| PubMed ID | 29269840 | Mgi Jnum | J:287479 |
| Mgi Id | MGI:6415821 | Doi | 10.1038/s41598-017-13678-5 |
| Citation | Ellenbroek GHJM, et al. (2017) Leukocyte-Associated Immunoglobulin-like Receptor-1 is regulated in human myocardial infarction but its absence does not affect infarct size in mice. Sci Rep 7(1):18039 |
| abstractText | 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 muL, p = 0.91 and end-systolic volume 112.1 +/- 22.2 vs. 106.9 +/- 33.5 muL, 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. |
