Fig. 6.

A model of the mechanism through which AhR mediates indoxyl sulfate-enhanced E-selectin expression via an activator protein-1 (AP-1)-dependent pathway. Indoxyl sulfate induces ROS production, which leads to TNF-α-triggered JNK and NF-κB activation. Indoxyl sulfate-induced AhR stimulates AP-1 transcriptional activity, but it is not associated with ROS production and JNK or NF-κB activation. AP-1 transcriptionally up-regulates E-selectin expression, followed by an increase in leukocyte-endothelial interactions.