Genome wide chromatin accessibilty changes associated with JUN expression in human normal and IPF lung fiborblasts

We found that JUN expression is increased in many human fibrotic diseases and that systemic induction of Jun in mice resulted in development of fibrosis of multiple organs. To identify the changes in chromatin accessibility associated with JUN, we worked with primary human fibrotic lung fibroblasts that have normal or Knock-out levels of JUN expression and performed ATAC-seq analysis in both of them. Meanwhile we also modified primary human normal lung fibroblasts with or without JUN over-expression induction, then processed ATAC-seq and ChIP-seq analysis. To confirm the key role of JUN in lung fibrosis process, chromatin accessibility and structure change profile in JUN gain-of-function and loss-of-function in primary human lung fibroblasts were evaluated by ATAC-seq and ChIP-seq using Nextseq 500.