Identification of differentially expressed miRNAs and key genes involved in the progression of alcoholic fatty liver disease using rat models

小桶 酒精性脂肪肝 基因 小RNA 代谢途径 基因表达 脂肪肝 生物 医学 计算生物学 转录组 生物信息学 疾病 遗传学 病理
作者
Xuemei Zhang,Wenqi Song,Mingxuan Zhang,Yuanhang Song,Yuzhu Di,Bo Chen,H. Tian,Xixian Yuan,Shizhu Jin
出处
期刊:Clinics and Research in Hepatology and Gastroenterology [Elsevier]
卷期号:46 (10): 102012-102012 被引量:1
标识
DOI:10.1016/j.clinre.2022.102012
摘要

Alcoholic fatty liver disease (AFLD) is a liver disease caused by prolonged heavy drinking and has a poor prognosis in the clinic. This study aimed to explore the differential miRNAs expression profiles in the AFLD rat model.The rat model of AFLD was established by ethanol intragastric administration and was used to explore the differential miRNAs expression profiles. We further analyzed the potential target mRNAs using the bioinformatics technique. GO and KEGG pathway enrichment analyses were carried out to better understand the biological function of differential expression genes (DEGs). We used the human Gene Expression Omnibus (GEO) dataset GSE28619 to further screen the key differentially expressed genes. The integration between the differentially expressed genes from the AFLD model and GEO was conducted and the key genes were identified.The serum ALT, AST, TG, and TC levels in the AFLD model group were significantly higher than those in the normal control group. There are 45 miRNAs with significant changes including 26 upregulated and 19 down-regulated miRNAs. GO and KEGG enrichment showed various metabolic processes and signaling pathways were enriched in the progression of AFLD. After integrating the results of GSE28619 and DEGs, we observed that there are 12 genes with significant changes in two data sets, including PSAT1, TKFC, PTTG1, LCN2, CXCL1, NR4A1, RGS1, VCAN, FOS, CXCL10, ATF3, and CYP1A1.AFLD showed differentially expressed miRNAs, which may be involved in the occurrence and progression of AFLD. Meanwhile, some signal metabolic pathways may be related to the pathogenesis of AFLD.
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