Genome wide chromatin accessibilty changes associated with JUN and SHH expression in human SSCL patients

We found that JUN and SHH 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 and SHH, we worked with primary SSCL dermal fibroblasts that have normal or Knock-out levels of JUN expression and vismodegib treatment then performed ATAC-seq analysis in all of them. Overall design: To confirm the key role of JUN and SHH in SSCL process, chromatin accessibility and structure change profile in JUN loss-of-function and vismodegib treatment in primary human SSCL dermal fibroblasts were evaluated by ATAC-seq using Nextseq 500.