Idiopathic pulmonary fibrosis (IPF) is a progressive, lethal fibrotic lung disease. IPF remains a major unsolved clinical problem with a median survival of 3 to 5 years. One reason for this is that currently available anti-fibrotic agents slow but do not arrest fibrotic progression. To arrest fibrotic progression, its obligatory drivers need to be identified.
These researchers have disovered intrinsically fibrogenic mesenchymal progenitor cells (MPCs) in the human IPF lung that are one source of IPF fibroblasts. IPF MPCs display a distinct transcriptome and a durable fibrogenic phenotype producing non-resolving interstitial pulmonary fibrosis when administered to immune-deficient mice. This suggests that IPF MPCs have undergone epigenetic modifications that underlie their pathologic function. The goal of this project is to identify global differences in the epigenome and transcriptome of IPF versus control MPCs by performing bulk RNA-seq and ATAC-seq.