2016
DOI: 10.1038/srep22613
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Silencing MicroRNA-155 Attenuates Cardiac Injury and Dysfunction in Viral Myocarditis via Promotion of M2 Phenotype Polarization of Macrophages

Abstract: Macrophage infiltration is a hallmark feature of viral myocarditis. As studies have shown that microRNA-155 regulates the differentiation of macrophages, we aimed to investigate the role of microRNA-155 in VM. We report that silencing microRNA-155 protects mice from coxsackievirus B3 induced myocarditis. We found that microRNA-155 expression was upregulated and localized primarily in heart-infiltrating macrophages and CD4+ T lymphocytes during acute myocarditis. In contrast with wildtype (WT) mice, microRNA-15… Show more

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Cited by 85 publications
(77 citation statements)
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“…Again, no circulating miRNAs were evaluated, limiting the meaningfulness of the results from a clinical perspective. The same miRNA was confirmed to play a major role in viral myocarditis, when miR-155 levels in mouse cardiac tissue were identified to increase during carditis in a macrophage dependent manner [130]. Another recent study found miR-221 and miR-222 as key regulators of the cardiac response to viral myocarditis [131].…”
Section: Infective Carditismentioning
confidence: 95%
“…Again, no circulating miRNAs were evaluated, limiting the meaningfulness of the results from a clinical perspective. The same miRNA was confirmed to play a major role in viral myocarditis, when miR-155 levels in mouse cardiac tissue were identified to increase during carditis in a macrophage dependent manner [130]. Another recent study found miR-221 and miR-222 as key regulators of the cardiac response to viral myocarditis [131].…”
Section: Infective Carditismentioning
confidence: 95%
“…Its depletion promotes M2 polarization and improves cardiac function following viral myocarditis [219]. This suggests that miRNA-155 might serve as a prognostic marker for cardiac death in post-MI patients [123].…”
Section: Summary: Non-coding Rnas and Immune Regulationmentioning
confidence: 99%
“…In viral myocarditis, the increased expression of miR-155 blocks macrophage polarization and alternatively activated M2 macrophages phenotype transformation. This results in increased pathogen induced inflammation and cardiac injury [142]. miR-155 also promotes macrophage survival by upregulating the SHIP1-Akt signaling cascade [143].…”
Section: Mirna and Cardiomyocytes Injurymentioning
confidence: 99%