Differentially expressed microRNA identification and target gene function analysis in starvation-induced autophagy of AR42J pancreatic acinar cells

作者：Gao, Bo; Wang, Duanping; Sun, Wang; Meng, Xianzhi; Zhang, Weihui^*; Xue, Dongbo^*

来源：Molecular Medicine Reports, 2016, 14(1): 590-598.

DOI：10.3892/mmr.2016.5240

• acute pancreatitis
• autophagy
• microRNA
• bioinformatics
• AR42J

Acute pancreatitis (AP) is a common acute digestive tract disease, with increased morbidity and mortality, and an unclear pathogenesis. Trypsinogen activation in pancreatic acinar cells may be the primary mechanism underlying the development of AP. Previous studies reported that autophagy participates in the formation of acinar cell vacuoles in AP and in the process of trypsinogen activation as an important cause of AP. Furthermore, microRNAs (miRNAs) maintain the autophagy process by regulating the expression of autophagy-associated genes. In the present study, an in vitro pancreatic acinar cell autophagy model was established using the AR42J starvation-induced pancreatic acinar cell line. Twenty differentially expressed microRNAs were identified using miRNA microarray. Bioinformatics analysis was used to predict the target genes of miRNAs and analyze the functions of differentially expressed miRNAs. The results demonstrated that only the downregulated miRNA rno-miR-148b-3p predicted 593 target genes with a statistical significance (P<0.05), from which 10 genes were autophagy-associated. The results of gene ontology and pathway analyses demonstrated that the target genes of miRNAs were enriched in the Response to insulin stimulus, Regulation of cell death and the Insulin signaling pathways (P<0.05, FDR<0.05). In addition, protein-protein interaction network analysis demonstrated a widespread interaction among the 593 target genes. The results of the present study may provide novel targets for research on the mechanisms of autophagy-promoted AP and AP treatment.

• 出版日期2016-7
• 单位哈尔滨医科大学