Basic Study
Copyright ©The Author(s) 2019. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Mar 7, 2019; 25(9): 1067-1079
Published online Mar 7, 2019. doi: 10.3748/wjg.v25.i9.1067
Integrated network analysis of transcriptomic and protein-protein interaction data in taurine-treated hepatic stellate cells
Xing-Qiu Liang, Jian Liang, Xiao-Fang Zhao, Xin-Yuan Wang, Xin Deng
Xing-Qiu Liang, Xiao-Fang Zhao, Department of Science and Technology, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning 530011, Guangxi Zhuang Autonomous Region, China
Jian Liang, College of Medical, Guangxi University, Nanning 530004, Guangxi Zhuang Autonomous Region, China
Xin-Yuan Wang, Xin Deng, School of Basic Sciences, Guangxi University of Chinese Medicine, Nanning 530200, Guangxi Zhuang Autonomous Region, China
Author contributions: Deng X and Liang XQ contributed equally to the study, performed the majority of experiments, and analyzed the data; Liang XQ wrote the paper; Zhao XF and Wang XY performed the treatment of HSCs; Liang J designed and coordinated the research.
Supported by the National Natural Science Foundation of China, No. 81360595 and No. 81860790; Guangxi Natural Science Foundation Program, No. KJT13066; the Bagui Scholars Foundation Program of Guangxi; the Special-term Experts Foundation Program of Guangxi; and the Project of Guangxi Young Teacher Fundamental Ability Promotion, No. 2017KY0298.
Institutional review board statement: The study was approved by the institutional review board of our hospital.
Institutional animal care and use committee statement: We did not use animals in our present study.
Conflict-of-interest statement: To the best of our knowledge, no conflict of interest exists.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Corresponding author: Xin Deng, MD, PhD, Professor, School of Basic Science, Guangxi University of Chinese Medicine, 13 Xianhu Avenue, Nanning 530200, Guangxi Zhuang Autonomous Region, China. 260446391@qq.com
Telephone: +86-771-2239080 Fax: +86-771-2239080
Received: December 5, 2018
Peer-review started: December 6, 2018
First decision: January 11, 2019
Revised: January 24, 2019
Accepted: January 26, 2019
Article in press: January 26, 2019
Published online: March 7, 2019
ARTICLE HIGHLIGHTS
Research background

Taurine is a beta amino acid with a simple structure and mostly appears in the free state in organism, and it plays a protective role against several forms of hepatic damage, including hepatic fibrosis. However, the molecular mechanism of taurine remains unclear, and therefore, it is difficult to use taurine for precision therapies in liver diseases.

Research motivation

The main topics of this study included investigating taurine-induced changes in gene expression in human HSCs, subjecting all of the differential expressed genes to gene ontology function and Kyoto encyclopedia of genes and genomes pathway enrichment analysis, exploring the interactions of differentially expressed genes (DEGs) in a human protein-protein interaction (PPI) network, and clarifying the mechanism of taurine on human hepatic stellate cells (HSCs). The findings enhance the understanding of the molecular mechanism of taurine-induced HSC apoptosis and provide references for liver disorder therapy.

Research objectives

The present study aimed to establish a network including transcriptomic and protein-protein interaction data, and to elucidate the molecular mechanism of taurine-induced HSC apoptosis.

Research methods

Raw microarray data were obtained as “.IDAT” and “.SDF” format using Genome Studio software (Illumina, San Diego, CA, United States), and then imported into the R environment for further processing. Subsequently, quantile normalization was carried out in R using the lumi package with Bioconductor open source software (http://www.bioconductor.org/). Significance was calculated using a t-test without multiple testing correction, selecting all transcripts with a minimum change in expression level of 1.5-fold together with a P-value less than 0.05. An enrichment analysis was then conducted using the Database for Annotation, Visualization and Integrated Discovery online tool, and the PPI network was constructed using Cytoscape software. Furthermore, the MCODE plug-in of Cytoscape was used to conduct a sub-module analysis.

Research results

It was found that nine critical genes, including MMP2, MMP9, MMP21, TIMP3, KLF10, CX3CR1, TGFB1, VEGFB, and EGF, were screened in the PPI network analysis.

Research conclusions

The present study showed that VEGFB, EGF, BDNF, TGFB1, FIGF, TIMP3, FGB, EGFR, F7, MMP9, MMRN1, and TCOF1 play key roles in the action mechanism of taurine, and these DEGs are mainly involved in positive regulation of protein kinase B signaling, ERK1 and ERK2 cascade, MAP kinase activity, MAPK cascade, cell migration, and cell proliferation.

Research perspectives

This study preliminarily explored the molecular mechanism of taurine on HSCs. Future studies should focus on the following aspects. First, the present study had no validation data and the findings could not be generalized to other conditions. As a result, future research should conduct the validate experiments, including the differentially expressed genes and the p38 MAPK-JNK-Caspase9/8/3 pathway by using blockers via the method of PCR and Western blot. Second, the characters of active and quiescent HSCs are different and the two subtypes should be studied separately in the future.