Chronic TCDD treatment increases liver myofibroblast activation through aryl hydrocarbon receptor signaling in hepatocytes

The goal of this project was to determine how AhR activity in hepatocytes and HSCs impact liver fibrosis by studying mice with AhR-deficient hepatocytes (AhRΔHep) or AhR-deficient HSCs (AhRΔHSC) during TCDD-induced liver fibrosis as measured by evidence of steatosis, inflammation, HSC activation, and collagen deposition. Overall, our studies indicate that chronic TCDD exposure increases AhR signaling in hepatocytes that result in indirect HSC activation and the development of liver steatosis, whereas hepatic inflammation do not appear to play a major role. Female AhRΔHep mice, AhRΔHSC mice, and AhRfl/fl mice were treated with 100 µg/kg TCDD or peanut oil every four days for 92 days and then euthanized. Treatment groups consisted of 3 mice. Overall 6 treatments can be found.