Deep sequencing analysis of microRNA expression in porcine serum-induced hepatic fibrosis rats

Aim. Recent studies have suggested miRNA dysregulation in liver tissue mediates the pathogenesis of various liver diseases especially liver fibrosis, but the microRNA changes during PS-induced hepatic fibrosis are still unknown. The purpose of this study was to screen the miRNA differences in rat li...

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Bibliographic Details
Main Authors: Shanfei Ge, Xiaowei Wang, Jianping Xie, Xin Yi, Fei Liu
Format: Article
Language:English
Published: Elsevier 2014-07-01
Series:Annals of Hepatology
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S1665268119308518
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Summary:Aim. Recent studies have suggested miRNA dysregulation in liver tissue mediates the pathogenesis of various liver diseases especially liver fibrosis, but the microRNA changes during PS-induced hepatic fibrosis are still unknown. The purpose of this study was to screen the miRNA differences in rat liver fibrosis model and clarify the relationship of miRNAs with the development of PS-induced liver fibrosis.Material and methods. Two fibrotic and two normal liver tissues from 20 Sprague-Dawley rats were collected and sequenced. MiRNA profiling results and fibrosis-related genes were validated by quantitative real-time polymerase chain reaction (qRT-PCR) and bioinformatics was used to predict miRNA targets.Results. In total, 48 miRNAs were detected to be aberrantly expressed in fibrosis tissue compared to normal tissue. Further functional analysis of the deregulated miRNA targets revealed the miRNAs are involved in several biological functions and pathways. In addition, the expression level of miR-27a and miR-146b and fibrosis-related genes were significantly up-regulated by using qRT-PCR in fibrotic liver tissues when compared to the normal liver tissues.Conclusion. PS-induced hepatic fibrosis results in up-regulation of the miR-27a and miR-146b in liver tissues, suggestingmiR-27a and miR-146b would be associated with the development of PS-induced liver fibrosis and be potential therapeutic targets during hepatic fibrosis.
ISSN:1665-2681