Bioinformatic analysis of miRNA expression patterns in TFF2 knock-out mice.
نویسندگان
چکیده
Trefoil factors, which bear a unique 3-loop trefoil domain, are a family of small secretory protease-resistant peptides (7-12 kDa) discovered in the 1980s. Trefoil factor 2 (TFF2) is a unique member of trefoil factors family that plays important roles in gastrointestinal mucosal defense and repair. However, few studies have characterized the miRNA expression patterns in TFF2 knock-out mice. In this study, we investigated the regulatory role of miRNAs in TFF2 knock-out mice. Whole miRNome profiling for TFF2 knock-out mice and wild-type mice were downloaded from the Gene Expression Omnibus database. A total of 14 differentially expressed miRNAs were identified using the limma package. Target genes for 2 differentially expressed miRNAs were retrieved from 2 databases. After mapping these target genes into STRING, an interaction network was constructed. Gene Ontology analysis suggested that the differentially expressed miRNAs are involved in cyclic AMP metabolism and the growth process. Additionally, dysregulated miRNAs target pathways of transforming growth factor-beta signaling pathway and cytokine-cytokine receptor interaction. Our results suggest that miRNAs may play important regulatory roles in processes involving TFF2, particularly in the regulation of signal transduction pathways. However, further validation of our results is needed.
منابع مشابه
Altered miRNA expression patterns in Tff2 knock-out mice correlate with cellular pathways of neoplastic development and caloric metabolism
The trefoil peptide family, consisting in mammals of three members namely TFF1, 2 and 3, plays a cytoprotective role in epithelial cells of various tissues, mainly in the digestive tract. Tff1, Tff2 or Tff3 knock-out mouse models developed various kinds of gastrointestinal impairment. microRNAs are known to be novel gene regulators. We aimed to investigate the physiological role of such miRNAs ...
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عنوان ژورنال:
- Genetics and molecular research : GMR
دوره 13 4 شماره
صفحات -
تاریخ انتشار 2014