| Literature DB >> 34632544 |
Tingjun Liu1, Jing Tong2, Chen Shao3, Junyan Qu4, Hua Wang1, Yi Shi2, Yajing Lin1, Yun Liu1, Shihe Shao5, Hongxing Shen6.
Abstract
Viral myocarditis (VM) is an inflammatory disease of the myocardium associated with heart failure, which is caused by common viral infections. A majority of the infections are initiated by coxsackievirus B3 (CVB3). MicroRNAs (miRNAs) have a major role in various biological processes, including gene expression, cell growth, proliferation, and apoptosis, as well as viral infection and antiviral immune responses. Although, miRNAs have been found to regulate viral infections, their role in CVB3 infection remains poorly understood. In the previous study, miRNA microarray results showed that miR-324-3p expression levels were significantly increased when cells and mice were infected with CVB3. It was also found that miR-324-3p downregulated TRIM27 and decreased CVB3 replication in vitro and in vivo. In vitro, analysis of downstream signaling of TRIM27 revealed that, miR-324-3p inhibited CVB3 infection, and reduced cytopathic effect and viral plaque formation by reducing the expression of TRIM27. In vivo, miR-324-3p decreased the expression of TRIM27, reduced cardiac viral replication and load, thereby strongly attenuating cardiac injury and inflammation. Taken together, this study suggests that miR-324-3p targets TRIM27 to inhibit CVB3 replication and viral load, thereby reducing the cardiac injury associated with VM.Entities:
Keywords: Coxsackievirus B3 (CVB3); TRIM27; Viral myocarditis (VM); miR-324-3p
Mesh:
Substances:
Year: 2021 PMID: 34632544 PMCID: PMC8692631 DOI: 10.1007/s12250-021-00441-4
Source DB: PubMed Journal: Virol Sin ISSN: 1995-820X Impact factor: 6.947