Zhao Wang, Jiangyang Sun, Yu Wang, Yichuan Zhang, Laian Ge
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引用次数: 0
Abstract
Background: Liver ischemia-reperfusion injury (IRI) is a common complication of diseases such as liver transplantation, hepatic resection, and hemorrhagic shock. This study aimed to elucidate the molecular mechanism of miR-107 affecting hepatic ischemia-reperfusion injury (IRI).
Methods: The expression changes of miR-107 during hepatic IRI were quantified using quantitative real-time PCR. Subsequently, in vitro cellular experiments were carried out to verify the role of miR-107 on hypoxia/reoxygenation (HR) through CCK-8, flow cytometer, and commercial kits. In terms of mechanism, it was determined that miR-107 had a regulatory relationship with target genes through luciferase reporter assay.
Results: In mouse liver IRI, miR-107 expression was increased while HMOX1 expression was decreased in liver tissues. In vitro cellular experiments, miR-107 inhibitors favored the alleviation of proliferation, apoptosis, inflammation, and oxidative stress in HR-damaged liver sinusoidal endothelial cells. In the molecular mechanism study, we determined that miR-107 could bind to HMOX1 and inhibit the HMOX1 expression. Low HMOX1 expression could eliminate the protective effect of miR-107 inhibitors.
Conclusion: MiR-107 expression was elevated during hepatic IRI and exacerbates hepatic injury by targeting HMOX1 inhibition.
HereditasBiochemistry, Genetics and Molecular Biology-Genetics
CiteScore
3.80
自引率
3.70%
发文量
0
期刊介绍:
For almost a century, Hereditas has published original cutting-edge research and reviews. As the Official journal of the Mendelian Society of Lund, the journal welcomes research from across all areas of genetics and genomics. Topics of interest include human and medical genetics, animal and plant genetics, microbial genetics, agriculture and bioinformatics.