Cardioprotection of M2 macrophages-derived exosomal microRNA-24-3p/Tnfsf10 axis against myocardial injury after sepsis.

Some reports have suggested the involvement of microRNA-24-3p (miR-24-3p) in heart diseases. Here, the intention of this work was to unmask whether miR-24-3p from M2 macrophages-derived exosomes (M2-exo) could protect against myocardial injury after sepsis. Mice model of sepsis was induced by intraperitoneal injection of lipopolysaccharide (LPS). miR-24-3p and tumor necrosis factor superfamily member 10 (Tnfsf10) expression levels were measured in the myocardial tissue of septic mice. M2-exo were isolated, in which miR-24-3p expression was altered. Then, septic mice were alone or in combination injected with the miR-24-3p-modified M2-exo or siRNA of Tnfsf10. Subsequently, cardiac function, apoptosis and serum inflammatory response were examined. miR-24-3p expression dropped while Tnfsf10 expression raised in the myocardial tissue of septic mice. M2-exo-derived miR-24-3p or deficiency of Tnfsf10 had cardioprotective effects on LPS-induced myocardial injury in mice through improving cardiac function and reducing cardiomyocyte apoptosis in the myocardial tissue and serum inflammation. A binding relation exhibited between miR-24-3p and Tnfsf10, and M2-exo-derived miR-24-3p alleviated LPS-induced myocardial injury by inhibiting Tnfsf10. Up-regulating miR-24-3p from M2-exo imposes cardioprotection against myocardial injury after sepsis through reducing Tnfsf10 expression. Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.

Citation

XingCheng Sun, Yuee Liu, Jin Wang, Min Zhang, Meitang Wang. Cardioprotection of M2 macrophages-derived exosomal microRNA-24-3p/Tnfsf10 axis against myocardial injury after sepsis. Molecular immunology. 2022 Jan;141:309-317

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PMID: 34933177

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