Overexpression of constitutively active Ikkb and/or loss of Stat3 in murine esophageal epithelium

Many esophageal diseases arise in the context of chronic inflammation, but the role that esophageal epithelial cells play in initiating inflammation remains poorly understood. Since the IKKβ/NF-κB and STAT3 pathways are critical signaling hubs that drive inflammatory-mediated responses, we aimed to identify how these two pathways regulate gene expression in esophageal epithelial cells. In this study, we performed RNA-Seq analysis on esophageal epithelium from mice with overexpression of constitutively active Ikkb and/or loss of Stat3 specifically in esophageal epithelial cells. Cre recombinase specific to esophageal epithelial cells (EBV ED/L2-Cre) was used to drive gene expression. We compared gene expression between control mice (ROSA26-STOPf/f-Ikk2ca; Stat3 f/f), mice with conditional overexpression of constitutively active IKKβ (ED/L2-Cre; ROSA26-STOPf/f-Ikk2ca), mice with conditional STAT3 knockout (ED/L2-Cre; Stat3 f/f), and mice with both conditional overexpression of active IKKβ and STAT3 knockout (ED/L2-Cre; ROSA26-STOPf/f-Ikk2ca; Stat3 f/f). Esophagi were harvested at 6 weeks of age for gene expression analysis.