Abstract 163: Interleukin-13 Expression Attenuates Left Ventricular Dilation and Mortality After Myocardial Infarction
Background: Monocyte infiltration and extracellular matrix breakdown/ de novo formation critically influence wound healing and remodeling after myocardial infarction (MI). Interleukin-13 (IL-13) has potent pro-fibrotic properties and is a differentiation factor for monocytes/ macrophages. Therefore, we studied whether IL-13 affects myocardial wound healing and remodelling after MI.
Methods and results: MI was induced by permanent ligation of the left coronary artery in WT and IL-13-/- mice. Expression of IL-13 was upregulated in the myocardium after MI. IL-13 expression was in part dependent on angiotensin II signalling as in vivo treatment with the Angiotensin-receptor blocker losartan attenuated myocardial IL-13 expression in response to MI. Intracellular FACS analysis of myocardial leukocytes further demonstrated IL-13 expression in a subset of myeloid CD11b+ cells within the myocardium. IL-13-/- mice showed higher mortality than WT mice after MI without difference in infarct size. Echocardiography further demonstrated increased left ventricular dilation in IL-13-/- when compared to WT mice. Histological analysis of the scar collagen did not reveal a difference between WT and IL-13-/- mice. FACS analysis of leukocytes from the infarct zone showed less MHC-II+ CD11b+ cells within the myocardium of IL-13-/- mice on day 7 indicating that IL-13 is required for the differentiation of heart infiltrating monocytes.
Conclusions: Expression of IL-13 in response to MI beneficially modulates wound healing after MI.
- © 2012 by American Heart Association, Inc.