Autor: |
Naveed Akbar, Abhirup Banerjee, Sam Dawkins, Robin P. Choudhury, Charlotte Lee, G Melling, Paul R. Riley, Keith M. Channon, Laurienne Edgar, Infarction Oam., Irina A. Udalova, Alastair L. Corbin, E Hogg, Mala Gunadasa-Rohling, R Dragovic, Daniel C. Anthony, David R. F. Carter |
Jazyk: |
angličtina |
Rok vydání: |
2021 |
Předmět: |
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DOI: |
10.1136/heartjnl-2019-bcs.224 |
Popis: |
Background Acute myocardial infarction (AMI) induces transcriptional activation of monocytes en route to the injured myocardium, in part driven by endothelial cell derived extracellular vesicles (EC-EV), which contain proteins and microRNA (miRNA) cargo. However, neutrophils are the first immune cells to arrive at sites of injury and mediate further damage to the ischemic myocardium. Here, we describe for the first time how neutrophils are released from the spleen in AMI and show that this is driven by EC-EV signalling. Methods and results Experimental AMI in wild-type mice caused a significant increase in peripheral blood neutrophils and a simultaneous reduction in splenic-neutrophil number (P Conclusions (I) Neutrophil deployment from the spleen is a novel finding in acute injury and interactions with (II) EC-EV may mediate their splenic liberation and (III) activation following AMI, en route to the injured myocardium. The splenic neutrophil reserve may be a novel therapeutic target in AMI to modulate the inflammatory response before recruitment of cells to sites of injury. |
Databáze: |
OpenAIRE |
Externí odkaz: |
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