2. Academic Validation
  3. Construction and Bioinformatics Analysis of ceRNA Regulatory Networks in Idiopathic Pulmonary Fibrosis

Construction and Bioinformatics Analysis of ceRNA Regulatory Networks in Idiopathic Pulmonary Fibrosis

  • Biochem Genet. 2024 Jun 13. doi: 10.1007/s10528-024-10853-y.
Menglin Zhang # 1 2 3,  Xiao Wu # 4,  Honglan Zhu 1,  Chenkun Fu 2,  Wenting Yang 1,  Xiaoting Jing 5,  Wenqu Liu 6,  Yiju Cheng 7 8
Affiliations

Affiliations

  • 1 Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, China.
  • 2 Department of Clinical Medicine, Guizhou Medical University, Guiyang, 550004, China.
  • 3 Department of Respiratory and Critical Care Medicine, People's Hospital of Anshun City Guizhou Province, Anshun, 561000, China.
  • 4 Department of Critical Care Medicine, The Second People's Hospital of Guiyang, Guiyang, 550004, China.
  • 5 Department of Respiratory and Critical Care Medicine, Guiyang Public Health Clinical Center, Guiyang, 550002, China. 46403043@qq.com.
  • 6 Department of Respiratory and Critical Care Medicine, People's Hospital of Anshun City Guizhou Province, Anshun, 561000, China. doctorququ@163.com.
  • 7 Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, China. chengchengyiju@126.com.
  • 8 Department of Respiratory and Critical Care Medicine, The Fourth People's Hospital of Guiyang, Guiyang, 550002, China. chengchengyiju@126.com.
  • # Contributed equally.
PMID: 38871957 DOI: 10.1007/s10528-024-10853-y
Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive form of pulmonary fibrosis of unknown etiology. Despite ongoing research, there is currently no cure for this disease. Recent studies have highlighted the significance of competitive endogenous RNA (ceRNA) regulatory networks in IPF development. Therefore, this study investigated the ceRNA network associated with IPF pathogenesis. We obtained gene expression datasets (GSE32538, GSE32537, GSE47460, and GSE24206) from the Gene Expression Omnibus (GEO) database and analyzed them using bioinformatics tools to identify differentially expressed messenger RNAs (DEmRNAs), MicroRNAs (DEmiRNAs), and long non-coding RNAs (DElncRNA). For DEmRNAs, we conducted an enrichment analysis, constructed protein-protein interaction networks, and identified hub genes. Additionally, we predicted the target genes of differentially expressed mRNAs and their interacting long non-coding RNAs using various databases. Subsequently, we screened RNA molecules with ceRNA regulatory relations in the lncACTdb database based on the screening results. Furthermore, we performed disease and functional enrichment analyses and pathway prediction for miRNAs in the ceRNA network. We also validated the expression levels of candidate DEmRNAs through quantitative real-time Reverse Transcriptase polymerase chain reaction and analyzed the correlation between the expression of these candidate DEmRNAs and the percent predicted pre-bronchodilator forced vital capacity [%predicted FVC (pre-bd)]. We found that three ceRNA regulatory axes, specifically KCNQ1OT1/XIST/NEAT1-miR-20a-5p-ITGB8, XIST-miR-146b-5p/miR-31-5p- MMP16, and NEAT1-miR-31-5p-MMP16, have the potential to significantly affect IPF progression. Further examination of the underlying regulatory mechanisms within this network enhances our understanding of IPF pathogenesis and may aid in the identification of diagnostic biomarkers and therapeutic targets.

Keywords

Differential expression analysis; Pulmonary fibrosis; ceRNA; lncRNA; miRNA.

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