Analysis of Microarray-Identified Genes and MicroRNAs Associated with Idiopathic Pulmonary Fibrosis

Author:

Fan Lichao12ORCID,Yu Xiaoting1ORCID,Huang Ziling1,Zheng Shaoqiang3ORCID,Zhou Yongxin4ORCID,Lv Hanjing5ORCID,Zeng Yu1ORCID,Xu Jin-Fu2ORCID,Zhu Xuyou1ORCID,Yi Xianghua1ORCID

Affiliation:

1. Department of Pathology, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China

2. Department of Respiratory and Critical Care Medicine, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai 200443, China

3. Department of Radiology, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China

4. Department of Thoracic-Cardiovascular Surgery, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China

5. Department of Respiratory Medicine, Shanghai Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China

Abstract

The aim of this study was to identify potential microRNAs and genes associated with idiopathic pulmonary fibrosis (IPF) through web-available microarrays. The microRNA microarray dataset GSE32538 and the mRNA datasets GSE32537, GSE53845, and GSE10667 were downloaded from the Gene Expression Omnibus (GEO) database. Differentially expressed miRNAs (DE-miRNAs)/genes (DEGs) were screened with GEO2R, and their associations with IPF were analyzed by comprehensive bioinformatic analyses. A total of 45 DE-microRNAs were identified between IPF and control tissues, whereas 67 common DEGs were determined to exhibit the same expression trends in all three microarrays. Furthermore, functional analysis indicated that microRNAs in cancer and ECM-receptor interaction were the most significant pathways and were enriched by the 45 DE-miRNAs and 67 common DEGs. Finally, we predicted potential microRNA-target interactions between 17 DE-miRNAs and 17 DEGs by using at least three online programs. A microRNA-mediated regulatory network among the DE-miRNAs and DEGs was constructed that might shed new light on potential biomarkers for the prediction of IPF progression.

Funder

Shanghai Municipal Natural Science Foundation

Publisher

Hindawi Limited

Subject

Cell Biology,Immunology

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