Potential function exploration of lncRNAs in idiopathic pulmonary fibrosis: insights from whole transcriptome sequencing data analysis

TL;DR

This study explores how long noncoding RNAs (lncRNAs) may contribute to idiopathic pulmonary fibrosis and identifies specific lncRNAs that could serve as biomarkers or treatment targets.

Contribution

The study identifies specific lncRNAs and their co-expressed mRNAs linked to inflammatory responses in idiopathic pulmonary fibrosis.

Findings

541 differentially expressed lncRNAs were identified in IPF, with 201 up-regulated and 340 down-regulated.

Six significant lncRNAs were found in modules correlated with IPF, and their co-expressed mRNAs were enriched in inflammatory response pathways.

Dysregulated lncRNAs and co-expressed mRNAs showed altered expression patterns in multiple cell types in IPF samples.

Abstract

•Long Noncoding RNAs (lncRNAs) played a role in Idiopathic Pulmonary Fibrosis (IPF).•Their specific functions and patterns of expression are still unclear.•The authors conducted a diagnostic study to study lncRNA functions in IPF.•lncRNAs were functionally active and potentially involved in inflammatory response.•Specific lncRNAs might be promising diagnostic biomarkers or therapeutic targets.

Long Noncoding RNAs (lncRNAs) played a role in Idiopathic Pulmonary Fibrosis (IPF).

Their specific functions and patterns of expression are still unclear.

The authors conducted a diagnostic study to study lncRNA functions in IPF.

lncRNAs were functionally active and potentially involved in inflammatory response.

Specific lncRNAs might be promising diagnostic biomarkers or therapeutic targets.

Research has shown that long noncoding RNAs (lncRNAs) play a role in Idiopathic Pulmonary Fibrosis (IPF), but their specific functions and patterns of expression are still unclear.

A diagnostic study was conducted by utilizing analysis techniques. RNA sequencing (RNA-seq) data from 12 IPF patients and 5 controls was used to study lncRNA functions in IPF. The authors identified Differentially Expressed lncRNAs (DElncRNAs) and explored co-expression networks in a transient manner, as well as using Weighted Gene Co-expression Network Analysis (WGCNA) to identify modules associated with IPF.

The study found 541 differentially expressed lncRNAs in IPF, with 201 up-regulated and 340 down-regulated. DElncRNAs, especially the up-regulated, were significantly correlated with DEmRNAs at their expression levels. DEmRNAs showed extracellular matrix-related biological functions in addition to increased lncRNAs. WGCNA results demonstrated that Module Eigengene green (MEgreen) and MEred modules indicated the highest negative correlation significance with IPF phenotype, and eigengene patterns of both modules were downregulated in IPF samples. The authors identified six significant lncRNAs in these two modules, including FAM13A-AS1, RP11–180C16.1, MYO16-AS1, AC007278.2, BACH1-IT2, and RP11–153M7.5, and their co-expressed DE mRNAs were enriched in inflammatory response pathways. The authors used single-cell RNA sequencing (scRNA-seq) data to investigate dysregulated lncRNAs and their co-expressed mRNAs. The authors found that five DEmRNAs that were co-expressed with DElncRNAs exhibited dysregulated expression patterns in multiple cell types of the IPF samples.

LncRNAs are functionally active and potentially involved in the inflammatory response in pathological processes of IPF. It is also important to consider some specific lncRNAs as potential diagnostic biomarkers or therapeutic targets for preclinical and clinical studies with IPF in the future.

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