Fibroblast histone deacetylase-1 promotes kidney interstitial fibrosis following ischemia-reperfusion injury.
Histone deacetylases (HDAC) are epigenetic regulators of trascription.  Preclinical studies have determined that HDAC inhibition can prevent kidney interstitial fibrosis in acute kidney injury.  The purpose of this study was to determine if overexpression of HDAC1 in kidney fibroblasts significantly affects the fibroblast transcriptome.  Transforming growth factor beta-1 (TGFB1) causes fibroblasts to differentiate into myofibroblasts leading to extracelluar matrix secretion.  A subset of our cells were treated with TGFB1 for 24 hours to determine if this in combination with HDAC1 overexpression significantly alters the transcriptomes. Overall design: Normal rat kidney fibroblast cells (NRK49F, ATCC) were transfected with either empty vector (pcDNA3.1) or human HDAC1-Flag plasmids (Addgene #13820, PMCID: PMC19648).  The cells were then treated with 2 ng/ml TGFB1 for 24 hours before RNA isolation and library preparation and sequencing.