Molecular pathogenesis involved in human idiopathic pulmonary fibrosis based on an integrated microRNA‑mRNA interaction network.

Idiopathic pulmonary fibrosis (IPF) is considered to be an ailment of the lungs that cannot be cured, wherein the lung tissues are characterized by increased thickness and stiffness, and/or scars. Despite the fact that extensive success has been achieved regarding the molecular diagnostics and pathobiology, the basic pathogenesis associated with IPF has not yet been fully elucidated and requires further clarification. In the current research, the changes in microRNA (miRNA) and mRNA expression in IPF were investigated through an integrative network technique. The authentic miRNA and mRNA expression profiling datasets were downloaded from Gene Expression Omnibus, followed by identification of differentially expressed miRNAs and mRNAs with use of the Significance Analysis of Microarrays algorithm. Expansion of the molecular targets associated with miRNAs was performed with the use of CyTargetLinker in Cytoscape, which was succeeded by validation with the use of mRNA array expression profiling. The incorporated miRNA-mRNA network covered 27 genes, in addition to 22 miRNAs that were associated with IPF development. As revealed by the functional enrichment analysis, the cytokine-cytokine receptor interaction and glycine, serine and threonine metabolism signalling pathways were extensively associated with IPF development. Overall, the present incorporated network illustrated the key link between miRNA and genes in IPF; in particular, it was elucidated that miR-409-5p and has-miR-376c, together with their target genes (C-C motif chemokine ligand 20 and oncostatin M), are likely candidates involved in the promotion of IPF initiation and progression.