The effects of S100A8/A9 blockade in experimental Myocardial Infarction detected by CITE-seq RNA sequencing

Abstract Background: The alarmin S100A8/A9, is released from neutrophils in response to inflammatory stimuli, but monocytes, and macrophages can also secrete extracellular S100A8/A9. During the acute phase of myocardial infarction (MI), S100A8/A9 site ischemic injury increases coronary systemic circulation. We have previously shown that plays an important role reparatory immune responses MI, blockade improves cardiac function post-MI. Methods: In present study we aimed understand, on local level, influence blockade, by sequencing 30,000 cells single-cell RNA (scRNA-Seq) CITE-Seq. MI mice were induced permanent artery ligation, followed blocker ABR-238901 or PBS for 3 days. CD45+ isolated blood, heart, bone marrow. Results: Cell populations blood generally reflected changes marrow detected shifts specific MI. reduced expression pro-inflammatory genes limited neutrophil monocyte sub-populations heart. treatment inhibited involved proliferation differentiation hematopoietic stem cells. Conclusions: has potent immunomodulatory effects through inhibition myelopoiesis population neutrophils, monocytes identified pathogenic heart could be therapeutically targeted reduce inflammation damage.