GSE210321
Identification of regulatory elements in primary sensory neurons involved in physical injury-induced neuropathic pain
Chronic pain is a significant public health issue that is often refractory to existing therapies. Here we combine ChIP-seq and ATAC-seq to identify cis-regulatory elements that show differential chromatin accessibility, and revealed transcription factor (TF) binding motifs with functionally regulation in the dorsal root ganglion (DRG) after nerve injury. We integrated RNA-seq to understand how differential chromatin accessibility after nerve injury may influence gene expression. We performed motif analysis of the differentially accessible H3K4me1 enriched regions to identify enrichment of TF motifs. Using TF protein arrays and ChIP-qPCR, we confirmed C/EBPg binding to a differentially accessible sequence and use RNA-seq to identify processes in which C/EBPg plays an important role. Our findings offer insights into those TF motifs that are associated with chronic pain. These data show how interactions between chromatin landscapes and TF expression patterns work together to determine gene expression programs in primary sensory neurons after nerve injury. Overall design: chromatin accessibility in naïve and injured, female rats