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MMP‐9 overexpression in macrophages regulates the post‐myocardial infarction inflammatory response through SCYE1

Post‐myocardial infarction (MI), proinflammatory macrophages secrete matrix metalloproteinase (MMP)‐9 to regulate the cardiac wound healing response. We hypothesized that overexpression of MMP‐9 in macrophages would amplify the inflammatory response to exacerbate left ventricular dysfunction post‐MI. Accordingly, we assessed function of the left ventricle (LV) in wild‐type mice (WT, n=16) and MMP‐9 macrophage‐specific transgenic mice (TG, n=28) at day 5 post‐MI. In response to similar infarct sizes of 49±2% for both WT and TG (p=0.9), LV ejection fraction was improved in the TG (25±2%) compared to the WT mice (18±2%; p<0.05). We also evaluated macrophage numbers by Mac‐3 and galectin‐3 levels and inflammatory cytokine gene expression. Despite a similar number of macrophages in both WT and TG, the expression of 23 inflammatory genes decreased in the infarct from the TG LV compared to WT LV (all p<0.05). Interestingly, SCYE1, a multifunctional cytokine involved in the regulation of inflammatory responses, was uniquely upregulated at baseline in TG (0.92±0.13 2−ΔCT units) compared to WT (0.52±0.07 units; p<0.05). SCYE1 levels decreased post‐MI in the TG (0.52±0.08 units) while WT levels doubled (1.02±0.16 units; p<0.05). The decrease in the TG levels of SCYE1 suggest that SCYE1 is a key MMP‐9 responsive regulator of the inflammatory response that follows MI.