Transcriptomic characterization of cardiac LECs and macrophages isolated from ACKR3∆Lyve1 and wild type mice with or without LAD ligation

In our study, we detected activation of ACKR3 signaling in cardiac lymphatics adjacent to the site of ischemic injury of left anterior descending artery (LAD) ligation. Furthermore, we found that Ackr3∆Lyve1 mice exhibited better survival and were protected from the formation of acute tissue edema after ischemic cardiac injury, in addition to a denser cardiac lymphatic network after LAD ligation, especially in the injured tissues. To characterize the transcriptomic changes in cardiac lymphatic endothelial cell (LEC) and macrophage populations in the heart upon ischemic cardiac injury in Ackr3∆Lyve1 mice, CD68+ macrophages and CD68-/LYVE1+ LECs were immunoprecipitated from the ventricles of Ackr3fl/fl and Ackr3∆Lyve1 mice at baseline or 7 days post LAD ligation. We then performed microarray on the collected lymphatic and macrophage RNA samples. CD68+ macrophages and CD68-/LYVE1+ lymphatic endothelial cells isolated from the hearts of male Ackr3∆Lyve1 and littermate control mice with or without LAD ligation. N=3 mice per group.