We studied the effects of 17β-estradiol (E2) (10, 40nM) on 2 vasoprotective pathways, i.e. cyclooxygenase-2 (COX-2)-dependent prostanoids and the antioxidant heme oxygenase-1 (HO-1), in human umbilical vein endothelial cells (HUVEC) exposed for 6h to steady laminar shear stress (LSS, 10dyn/cm2), characteristic of atherosclerotic lesion-protected areas. COX-2 was induced by LSS versus static condition (SC). E2 did not significantly affect COX-2 expression in HUVEC cultured in SC or exposed to LSS. Prostacyclin (PGI2) and prostaglandin (PG)E2 were induced while PGF2α was reduced by LSS. E2 caused no effect or a small reduction of prostanoid biosynthesis. In HUVEC cultured in SC or exposed to LSS, E210nM caused a comparable HO-1 induction (35–45%) while E2 40nM was 5-fold more potent in LSS-exposed HUVEC than in SC (290% and 58%, respectively). PGI2 receptor antagonist RO3244794 did not affect HO-1 induction by E2. In conclusion, E2 may restrain oxidant stress in the endothelium through HO-1 induction by a mechanism independent on PGI2 signaling.
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