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Figure S3. Schematic of COX-2 regulation of TF expression in ECs. EC COX-2 and PGIS enzymes catalyze the oxidative reactions in the conversion of the endocannabinoid 2-AG to PGI2-glycerol ester. PGI2 and related prostanoids are potent activators of PPARδ. Data in this report demonstrate that this signaling pathway inhibits the expression of TF, which is a critical prothrombotic factor. Both basal- and inflammatory signal-induced (e.g., LPS that activates the Toll-like receptors) expression of TF is attenuated by the COX-2-PPARδ pathway. Treatment of ECs with PPARδ activators or 2-AG suppressed TF expression, thus providing alterative ways of alleviating coxib-induced thrombotic complications.