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Identification of IPF Specific Genes Expressed by Lung Tissue - Derived Fibroblasts Using Next Generation Sequencing

ABSTRACT: This study presents transcriptomic profiling of primary lung fibroblasts derived from patients with idiopathic pulmonary fibrosis (IPF) and histologically normal controls. Total RNA sequencing was performed to identify differentially expressed genes associated with fibroblast activation in IPF. A total of 43 samples (33 IPF and 10 controls) were analyzed. The results revealed robust gene expression changes in IPF fibroblasts, with significant enrichment in extracellular matrix organization and collagen-related pathways. This dataset provides a valuable resource for understanding the molecular landscape of IPF fibroblasts and may facilitate the identification of novel biomarkers and therapeutic targets.

ORGANISM(S): Homo sapiens

PROVIDER: GSE301181 | GEO | 2026/05/15

REPOSITORIES: GEO

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Project description:The activated fibroblast is the central effector cell for the progressive fibrotic process that characterizes idiopathic pulmonary fibrosis (IPF). An understanding of the genomic phenotype of this cell in isolation is essential to the understanding of disease pathogenesis and is integral to strategizing therapeutic trials. Employing a unique technique that minimizes cellular phenotypic alterations, we characterized the genomic phenotype of non-cultured pulmonary fibroblasts from the lungs of patients with advanced IPF. This approach revealed several novel genes and pathways previously unreported in IPF fibroblasts. Specifically, we demonstrate altered expression in proteasomal constituents, ubiquitination mediators, the Wnt pathway and several cell cycle regulators suggestive of loss of normal cell cycle controls. The pro-inflammatory cytokine CXCL12 was also up-regulated which may provide a mechanism for fibrocytes’ recruitment, while up-regulated oncogenic KIT may promote fibroblast over proliferation. Paradoxically, pro-apoptotic inducers such as death inducing ligand TRAIL (TNFSF10) and pro-apoptotic Bax were also up-regulated. This comprehensive description of altered gene expression within IPF fibroblasts sheds further light on the complex interactions that characterize IPF. Further studies including therapeutic interventions directed at these pathways hold promise for the treatment of this devastating disease. 58 samples of total RNA isolated from 12 lungs of patients with end-stage idiopathic pulmonary fibrosis and 6 donors of normal lungs (controls) who were designated brain dead, non-diseased donors whose lungs failed criteria for transplantation and who were organ donors for research. RNA extraction followed the Qiagen RNeasy Kit using QIshredder columns for shredding of DNA contiminants. Experimental/control samples were amplified amino-allylated RNA labeled with Cy5 and Stratagene Reference RNA was amplified and amino-allylated and labeled with Cy3. Amplification was one round using Ambion MessageAmp II kit with amino-allylated UTP according to the protocol of the Duke University Institute for Genome Sciences and Policy. Amplification and amino-allylation of the Stratagene Reference RNA and Hybridization of Reference with patient samples and controls was done by the Duke Institute for Genomic Sciences and Policy.

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Identification of IPF Specific Genes Expressed by Lung Tissue - Derived Fibroblasts Using Next Generation Sequencing

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