Treatment with the IL-2 complex significantly attenuated ventricular remodeling, reduced infarct size, and improved left ventricular function in mice after myocardial infarction.
Does the IL-2 complex attenuate cardiac remodeling after myocardial infarction in a mouse model?
The IL-2 complex attenuates adverse cardiac remodeling after myocardial infarction in mice by expanding regulatory T cells and promoting M2 macrophage differentiation.
CD4+CD25+Foxp3+ regulatory T cells (Treg cells) have protective effects in wound healing and adverse ventricular remodeling after myocardial infarction (MI). We hypothesize that the interleukin- (IL-) 2 complex comprising the recombinant mouse IL-2/anti-IL-2 mAb (JES6-1) attenuates cardiac remodeling after MI through the expansion of Treg. Mice were subjected to surgical left anterior descending coronary artery ligation and treated with either PBS or IL-2 complex. The IL-2 complex significantly attenuates ventricular remodeling, as demonstrated by reduced infarct size, improved left ventricular (LV) function, and attenuated cardiomyocyte apoptosis. The IL-2 complex increased the percentage of CD4+CD25+Foxp3+ Treg cells, which may be recruited to the infarcted heart, and decreased the frequencies of IFN-γ- and IL-17-producing CD4+ T helper (Th) cells among the CD4+Foxp3- T cells in the spleen. Furthermore, the IL-2 complex inhibited the gene expression of proinflammatory cytokines as well as macrophage infiltrates in the infarcted myocardium and induced the differentiation of macrophages from M1 to M2 phenotype in border zone of infarcted myocardium. Our studies indicate that the IL-2 complex may serve as a promising therapeutic approach to attenuate adverse remodeling after MI through expanding Treg cells specifically.
Zeng et al. (Fri,) conducted a other in Myocardial Infarction. Interleukin-2 (IL-2) complex vs. PBS was evaluated on Ventricular remodeling (infarct size, left ventricular function, and cardiomyocyte apoptosis). Treatment with the IL-2 complex significantly attenuated ventricular remodeling, reduced infarct size, and improved left ventricular function in mice after myocardial infarction.