Fig. 3

The AHR non-genomic pathways. After exogenous ligand TCDD binds to AHR, calcium ions from the extracellular and endoplasmic reticulum enter the cytoplasm, resulting in increased intracytoplasmic calcium ion concentration rapidly, which causes the activation of PKCα, the phosphorylation of PLA2 and the subsequent production of arachidonic acid. At the same time, the binding of TCDD to the AHR results in the release of tyrosine kinase Src from the AHR complex. The activation of Src could be accompanied by the activation of the FAK and the modification of the adhesion properties. The activation of Src could also directly lead to the rapid activation of MAPK signaling pathways. Next, the activation of MAPK by Src leads to the transcription of COX2, and it can use arachidonic acid to produce prostaglandins which can cause inflammation. At last, these two TCDD-activated signaling pathways ultimately converge toward the stimulation of inflammation