Identification of key genes associated with idiopathic pulmonary fibrosis using bioinformatics analysis

Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal interstitial lung disease. The goal of this study is to elucidate the molecular mechanism of IPF. GSE24206 was downloaded from Gene Expression Omnibus, which included 17 IPF and 6 control samples. The t-test was applied to identify differentially expressed genes (DEGs) between IPF and control samples. Pathway and functional enrichment analyses were used to investigate the functions involving these DEGs. According to the information of TRANSFAC, Tumor Associated Gene (TAG) and Tumor Suppressor Gene (TSGene) databases, the screened DEGs were further annotated. To comprehensively understand the interactions between proteins encoded by the DEGs, protein-protein interactions (PPIs) were predicted by STRING and PPI network was visualized by Cytoscape software. Additionally, module analysis for PPI network was performed using BioNet tool. Total 192 up-regulated and 28 down-regulated genes were identified. Both down-regulated PDGFRA and up-regulated CCND1 were TAGs. Pathway enrichment analysis indicated that PDGFRA were involved in all of the 8 pathways for the 28 down-regulated genes. Besides, LTBP3 andTHY1 separately were involved in extracellular matrix organization and cell adhesion. After PPI network analysis, we discovered that the degree of COL1A2, TGFB1, COL1A1, COL3A1, ASPN, CD4, SDC1, CXCL12, COL5A1, and COMP were significantly higher. In conclusions, our results showed that the pathology of IPF involved multiple dysregulated genes, and our study would pave ways for further study of IPF.